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The Spleen 

Edited By 

Andy Petroianu 

Professor of Surgery, Department of Surgery, School of Medicine, 

Federal University of Minas Gerais, Belo Horizonte 

Brazil

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DEDICATION 

I offer this splenic bouquet as a tribute to my father, Jac, who inspired me to begin and 

persist in my studies on the spleen and who was the paradigm of my conduct. 

I offer these flowers in the honour of my mother, Sonia, the strong pillar of our family. 

I dedicate each petal to my daughter, Larissa, the main reason of all purposes of my life.

CONTENTS 

Foreword i 

Preface ii 

List of Contributors iii 

CHAPTERS 

1. Historical Aspects of Spleen and Splenic Surgeries 


3 

2. Functions of the Spleen and their Evaluation 

Catalin Vasilescu 

20 

3. Histology and Histopathology of the Spleen 

Kim Vaiphei 

37 

4. Some Aspects of Splenic Pathology 

Alfredo J. A. Barbosa 

75 

5. Sepsis and the Spleen 

Ruy Garcia Marques 

84 

6. Surgical Anatomy of the Spleen 


117 

7. The Spleen in Patients with Portal Hypertension 

Ahmed Helmy 

134 

8. Benign Vascular, Cystic and Solid Diseases of the Spleen 

Eelco de Bree, Vasilis Charalampakis and John Melissas 

153 

9. Chronic Lymphocytic Leukemia, Follicular Lymphoma and the Spleen 

André Márcio Murad and Andy Petroianu 

179 

10. Primary and Metastatic Cancer of the Spleen 

Jörg Sauer 

192 

11. Pre- and Postoperative Care for Surgical Procedures on the Spleen 

Mircea Dan Venter 

201 

12. Conservative Surgical Procedures on the Spleen 


217 

13. Laparoscopic Splenectomy 

René Berindoague Neto 

250 

14. Robotic Splenectomy 


259 

15. Splenic Trauma 

Takeshi Shimazu 

264 

Index 276

FOREWORD 

I welcome this work with enthusiasm. Having devoted most of my professional life to study the spleen and to 

research on techniques of splenic resection, I was pleased and honored when the editor of this book, Dr. Andy 

Petroianu, asked me to write a foreword to it. Books solely on the spleen are relatively rare and books on splenic 

surgery are even rarer. Among human solid organs, the spleen seems to be an orphan. With most other organs, such 

as the brain, heart, and kidney, much has been written on their history, anatomy, function and surgical treatment. An 

up-to-date volume on the current concepts and techniques of splenic surgery is the most necessary and 

commendable addition. 

Why has the spleen lagged behind other organs in published works? In the popular mind, many people are unaware 

that they even have a spleen. Still others do not know where in the body it is located. Almost no one knows what it 

does. For surgeons, it has long been a bête noir, accessible only with difficulty high in the left upper quadrant and so 

fragile that even minor inadvertent injury could lead to lethal hemorrhage. That this is no longer true which is amply 

written about in this book by a group of international experts in splenic disease and splenic surgery. 

Modern splenic surgery owes its spectacular rise partially to advances in other fields. In the diagnosis of splenic 

diseases, the explosive growth of imaging capabilities has been added immensely to our capabilities. These have 

included radionuclide scanning, ultrasound, computerized tomography and magnetic resonance imaging. They all 

contributed to elucidating difficult diagnostic problems. New hemostatic techniques can also be credited, since the 

spleen is so unforgivably fragile and subject to obstinate and dangerous bleeding. For this problem, there were 

advances such as electro cautery, stapling, argon beam, high frequency ultrasound and a great variety of topical 

hemostatic agents such as fibrin glue, microfibrillar collagen and a host of others. Finally, the laparoscopic 

revolution has been truly transformative. Frankly, when it was first mentioned to me, I was incredulous as I recalled 

my many years of struggle in the left upper quadrant with the abdomen open. To think that all of that could be 

accomplished remotely through a narrow tube was beyond my imagination. I was proven wrong in my own 

institution when bold surgeons looked past my doubts and were among the first to perform and publish on 

laparoscopic splenectomy. It has now become the standard of care for many splenic diseases. 

What is there to look forward to some future edition of this book on the same subject material? Predictions are 

always dangerous but are good mental exercises and sometimes come true. I think that a number of diseases now 

requiring splenectomy will be eliminated by advances in genomic medicine, targeted chemotherapy and stem cell 

therapy and other new approaches. Splenectomy in the leukemias will become increasingly rare or non-existent. 

Witness, for example, the success of Gleevec for myelogenous leukemia and the purine analogues for hairy cell 

leukaemia. Splenectomy for metabolic diseases like Gaucher Disease will also become rarer. Witness the success of 

the replacement enzyme, glucocerebrocidase. Splenectomy for parasitic diseases will yield to specific therapies as 

they are discovered. Splenectomy for a malignant neoplasm such as Hodgkin’s Lymphoma has virtually disappeared 

and other tumors will also be conquered as the cure or cures for cancer are found. Splenectomy for benign 

neoplasms such as hemangioma will yield to better diagnosis and conservative surgery. 

I also believe that the technique of laparoscopic splenectomy will be enhanced by three dimensional imaging, zoom 

capabilities and texture detecting technology. There will also be new hemostatic manoeuvres and topical agents that 

will ease the bleeding problem. Finally, I am convinced that conservative surgery of the spleen will become the 

standard of care world-wide, it is an organ that is much better left in than taken out. 

This book serves the purpose of a comprehensive survey and description of the current state of the art of splenic 

surgery. It is timely, necessary and indeed welcome. 

i 

Leon Morgenstern 

UCLA School of Medicine, 

Califórnia

ii 

PREFACE 

The spleen is one of the most important organ, and is responsible for many pivotal functions, such as defense of the 

organism, the removal of foreign particles from the blood flow, the metabolism of bilirubins, lipids and several 

aminoacids, the control of the number of blood leukocytes and platelets, the maturity of lymphocytes and opsonins, 

hematopoesis, among others. Thus, this organ belongs to several medical specialties, mainly Haematology, 

Immunology, Oncology, Infectology and Surgery. 

Splenectomy is a general surgical procedure which is most commonly used in trauma, but it is also performed to 

treat haematological, immunological, metabolic and oncological diseases. Other indications for splenectomy include 

morphological disturbances, retarded somatic and sexual development, portal hypertension, parasitic infections, 

abscesses haemangiomas and cysts. 

Until recently, the absence of the spleen was not considered as a risk factor for severe complications, even with the 

knowledge of death provoked by postsplenectomy sepsis, which has existed since the nineteenth century. Recent 

studies have proved that the complete removal of the spleen is mostly useless, and is commonly followed by a high rate 

morbidity and mortality. Moreover, asplenic patients are more susceptible to severe infections, including overwhelming 

sepsis, meningitis and pneumonia. The estimated incidence of severe sepsis after total splenectomy is 8%. 

Another critical postsplenectomy complication is pulmonary thromboembolism. The incidence of this affection may 

reach 35%. This complication is apparently not due to thrombocytosis, although the number of platelets may 

increase considerably in asplenic patients. 

Haematological diseases, such as myeloid hepatosplenomegaly, leukemias and lymphomas, as well as metabolic 

affections, including dyslipidemias, are followed by high morbidity and mortality rates when the spleen is removed. 

In these cases, conservative surgeries are proposed to avoid this problem. On the other hand, total splenectomy may 

be inevitable in cases such as trauma or even in elective conditions (eg. hypersplenism, idiopathic thrombotic 

purpura, spherocytosis, among others). The benefits generated by this procedure must be weighed against the risks 

of asplenism. 

This book is written exclusively to show the spleen in relation to basic sciences (anatomy, physiology) and the 

clinical practice of specialties related to this organ is useful for clinical physicians, haematologists, oncologists, 

infectologists, general surgeons, oncologic surgeons, trauma surgeons, resident physicians and medical students. 

The Bentham Science Publishers gave the honour of editing this book. I am proud to accept the challenge and have 

the privilege of bringing together distinguished researchers from several countries on medical procedures concerning 

the spleen. Professor Leon Morgenstern, who is the most esteemed reference in studies regarding the spleen agreed 

to write the foreword of this book. All participating authors have written pivotal chapters and have contributed to 

advances in research on medical procedures concerning the spleen. Thanks to these contributors, as well as, many 

other investigators around the world, the spleen is no longer as mysterious as it was once described by Claudius 

Galen. 


Federal University of Minas Gerais, 

Brazil

Ahmed Helmy 

LIST OF CONTRIBUTORS 

Associate Professor and Consultant, Director of Viral Hepatitis Services and Research Centre of the Department of 

Tropical Medicine and Gastroenterology, Faculty of Medicine of the Assiut University Hospitals, Egypt 

Alfredo José Afonso Barbosa 

Professor of the Department of Pathology, School of Medicine, Federal University of Minas Gerais, Belo Horizonte, 

Brazil 

André Márcio Murad 

Associate Professor of the Department of Clinics and Medical Oncology of the School of Medicine, Federal 

University of Minas Gerais, Brazil 


Professor of Surgery of the Department of Surgery of the School of Medicine of the Federal University of Minas 

Gerais, Belo Horizonte, Brazil 

Avenida Afonso Pena 

Belo Horizonte, MG 30130-005, Brazil 


Associate Professor of the Fundeni Institute of Digestive and Liver Transplantation, 258 Fundeni Street - Bucharest, 

Romania 

Eelco Bree 

Associate Professor of Surgical Oncology, University Hospital, Heraklion, Greece - P.O. Box 1352, Heraklion 

71110, Greece 

J. Melissas 

Professor of Surgery and Head of the Department of Surgical Oncology, University Hospital, Heraklion, Greece - 

P.O. Box 1352, Heraklion 71110, Greece 

Jörg Sauer 

Professor of Surgery, Karolinen-Hospital Hüsten, Department of General and Visceral Surgery - D-59759 Arnsberg, 

Germany 

Kim Vaiphei 

Additional Professor of the Department of Histopathology, PGIMER Chandigarh, India 

Mircea Dan Venter 

Associate Professor of the Department of Surgery of the Emergency Clinical Hospital, Bucharest, Romania 

René Berindoague Neto 

Associate Professor of the Faculty of Medical Sciences of Minas Gerais and Surgeon of the Institution of Teaching 

and Research of the Holly House of Misericorde of Belo Horizonte, Brazil 

Rua dos Otoni 

909 - sala 404 - Belo Horizonte, 30150-221, Brazil 

iii

iv 


Associate Professor of the Department of Surgery of the School of Medicine, State University of Rio de Janeiro, Rio 

de Janeiro, Brazil 

Takeshi Shimazu 

Professor of Surgery of the Department of Traumatology and Acute Critical Medicine of the Faculty of Medicine 

(D-8) of the Osaka University - (D-8) 2-15 Yamadoaka, Suite-shi, Osaka 565-0871 

Vasilis Charalampakis 

Associate Professor of Surgical Oncology, University Hospital, Heraklion, Greece - P.O. Box 1352, Heraklion 

71110, Greece

Historical Aspects of Spleen and Splenic Surgeries 

Andy Petroianu* 

The Spleen, 2011, 3-19 3 

Department of Surgery of the Federal University of Minas Gerais, Belo Horizonte, Brazil 

". Advance our standards; Inspire us with the spleen of fiery dragons!Victory sits on our helms." 

Andy Petroianu (Ed) 

All rights reserved - © 2011 Bentham Science Publishers Ltd. 

CHAPTER 1 

William Shakespeare - King Richard III, act 5, scene 3. 

Abstract: Since Antiquity, the spleen has been fascinating due to the mysteries of its existence and, to date, this 

is the organ about which we know the least. The most ancient documentation of the spleen comes from the 

Chinese. Throughout history, many functions have been attributed to the spleen. For a more didactic presentation, 

this chapter will be divided into three larger topics, in which the historical aspects of the spleen – Morphology, 

Physiology and Surgery – will be treated. Great advances in splenic morphology are due to Marcelo Malpighi. 

His outstanding studies on the spleen, around 1686, resulted in the knowledge of the splenic capsule and its 

intraparenchymatous insertions, in a trabecular form. The first study on the vascular pedicle of the spleen is 

attributed to Julius Caesar Arantius, in 1571. The greatest importance attributed to the spleen is the protection of 

the organism against infections. Hua T'o, had performed a full splenectomy in the second century a.D. in China. 

The first splenectomy described in detail was carried out by Adrian Zaccarelli, in 1549. The first partial 

splenectomy may have been performed in 1581. In 1590, Dr. Viard used a string to stitch a segment of the spleen 

that had come become exposed due to a small abdominal wound and performed the first partial splenectomy. The 

first description of the splenic implant in the peritoneum, after a human trauma, was reported by H. Albrecht 

(1896), in Germany. In 1985, Salky et al., considered that the decapsulation of the non-parasitic splenic cyst by 

laparoscopy was the definitive treatment for this disturbance. The authors of the first total splenectomy executed 

by laparoscopy most likely belong to Delaitre and Maignien (1991). Only with persistent study can the spleen 

cease to be, in the words of Galen (second century), “an organ full of misteries”, "mysterii pleni organon". 

Key Words: Spleen, History, Surgery, Pathophysiology, Morphology, Physiology, Complications, Anatomy. 

INTRODUCTION [1-9] 

Since Antiquity, the spleen has been fascinating due to the mysteries of its existence and, to date, this is the organ 

about which we know the least. On the other hand, even without a reasonable explanation for our current 

comprehension, many peoples throughout the ages have attributed functions to the spleen, which, centuries later, 

science could prove to be true. It is quite amazing how the ancient philosophers, with no resources other than that of 

observation, described the spleen quite accurately, in both morphological and functional aspects. 

The most ancient documentation of the spleen comes from the Chinese. In traditional Chinese Medicine, the spleen 

is one of the four organs of the body and is related to the defence of the organism, the supply of energy from other 

organs and digestion. In fact, the spleen performs all of these functions, and since it represents 25% to 30% of the 

phagocyte mononuclear system, it is responsible for the removal of antigens from circulation. The splenic 

macrophages phagocyte bacteria, viruses and fungi, even without the presence of opsonins. This organ produces 

lymphocytes, all of the immunoglobulins, as well as the diverse peptides that are important within the organism 

immune system defences. The energy described by the Ancient Chinese can be represented by the red blood cells 

that the spleen releases into the circulation of many mammals in situations which require a greater systemic effort. 

As regards the role of the spleen in digestion, two aspects should be considered. First, the spleen is the precursor of a 

great majority of hepatocyte functions, such as the formation of bilirubins, and takes part in the formation cycles of 

peptides and lipids. The second aspect is of microscopic digestion, which is exercised by splenic macrophages. 

*Address correspondence to Andy Petroianu: Avenida Afonso Pena, 1626 - apto. 1901, Belo Horizonte, MG 30130-005, Brazil; Tel / Fax: 55- 

31-3274-7744; E-mail: petroian@gmail.com

4 The Spleen Andy Petroianu 

In the Hebrew culture, the spleen received the name of techol. According to Talmud and Midrash, books on historical 

traditions, this organ was responsible for producing laughter and happiness, but also played the role of the mill, with the 

function of grinding down impurities within the blood. In Zohar, the book which governs the kabala, Hebrew mysticism, 

describes the spleen as one of the ten organs which contains the spirit and which is responsible for happiness. Also 

within Hebrew history is the first reference to the splenectomy. It tells that, in the days of King David, approximately 

three thousand years ago, the spleens of fifty soldiers from the troops of Adoniah were removed so that they could run at 

greater speeds. In this time, it was also believed that the spleen was responsible for lethargy and indolence. 

It is not absurd to attribute the functions of purifying the blood and “producing happiness” to this organ, since all 

diseases, especially those of septic origin, are followed by a fall in one’s general state of being, coupled with a lack 

of appetite and “sadness”. Therefore, the happiness promoted by the spleen would be intermediated by one’s health 

and by the well-being stemming from the purification of the blood, removing noxious substances from the organism. 

On the other hand, lethargy and indolence are linked to anaemia. If we consider that in ancient times malaria and 

Manson’s schistosomiasis were endemic diseases throughout the Middle East, it is reasonable to presume that the 

splenomegaly, present in all illnesses, caused anaemia by means of an increased storage of blood. 

As regards the splenectomy, it is highly unlikely that this actually existed in those days, as there is no record in the old 

world that describes this type of surgery or figure that presents some type of abdominal scar in the region of the spleen. It 

is also quite odd that the removal of the organ related to the purification of the blood and happiness can lead to a better 

physical performance. However, as mentioned above, the population of the Middle East was at the mercy of endemic 

diseases, which cause splenomegaly and anaemia, with a consequent abdominal discomfort and adynamia. Therefore, if 

the splenectomy had been performed, it would certainly have increased the performance of the warriors. Another subsidy 

of the greater physical development of those who underwent splenectomies stems from research carried out by Schulz 

(1828) and by Macht and Finesilver (1922), who found that splenectomised mice presented greater speed and resistance 

in races as compared to animals, who had intact spleens. In an experimental study with rats, we verified that the animals 

without spleen ran faster and during a longer period than the controls with spleen. 

In Sanscript, the Indo-European language which gave origin to the majority of the Western languages, including 

Greek, Latin and Germanic, the name for the spleen was plihan or plihaa. This may well be the origin of 

(splén), spleen in Greek, a word which may also find its origin in the term (splanchnon), 

which means viscous, with no shine, offal (gave origin to splanchnic), or (spao), to remove. Viscous and pale 

can also be written as (bádios), which is the Greek adjective for spleen. These words reveal that the Greek 

saw this organ as an offal with an opaque aspect, as it had the function of removing the impurities of the blood. It is 

presumed that, upon conquering the Hebrews, the Greek incorporated the functional concepts of the spleen, as well 

as the idea that the splenectomy could improve the performance of athletes. By removing the letters “sp” from splén, 

the word lien was formed, the name given to the spleen by the Romans. 

In the Teutonic language of the ancient Germanic peoples, the spleen was designated as milt, which means to digest. This 

word originated from Milz, in German; and later mjelte, in Norwegian; melta, in Icelandish; milza, in Italian. In all of 

these languages, the concept of digesting food was maintained, most likely due to the proximity of the spleen to the 

stomach. However, it is interesting to note that the word mjelte from Norwegian also means “fish egg”, most likely due 

to the similarity between the form of the spleen in some animals and the sack of eggs found in the abdomen of fish. 

We were unable to find the origin of the word rate, which means spleen in French. In the English and Romanian 

languages, the word spleen and splinã, which mean spleen, find their origins in the Greek noun (splén). 

However, the bazo in Spanish and baço in Portuguese and originate directly from the Greek adjective 

(bádios), maintaining its double meaning: offal and of viscous, opaque or pale. 

Throughout history, many functions have been attributed to the spleen, of which the following deserve to be mentioned: 

refuge of emotions and passions; 

source of laughter, happiness and delight; 

organ responsible for attacks of anger, maliciousness and ill-temper;

Historical Aspects of Spleen and Splenic Surgeries The Spleen 5 

origin of sudden impulses; 

offal which gives refuge to pride, courage and impetus; 

garnered of veiled evil and disrespect; 

organ that removes melancholia and depression; 

producer of blood; 

purifier of the blood; 

deposit of energy; 

responsible for the digestion of food, etc. 

Setting aside the legends and impressions about the spleen, it should be noted that this organ has also been the target 

of much research, which resulted in the current knowledge concerning this offal. For a more didactic presentation, 

this chapter will be divided into three larger topics, in which the historical aspects of the spleen – Morphology, 

Physiology and Surgery – will be treated. 

SPLENIC MORPHOLOGY [1,3-8,10-15] 

Erisistratus de Chios, who lived in Alexandria, in the third century A.C., is considered to be the founder of 

Anatomy, because of his works on the symmetry of organs. According to his works, the only function of the spleen, 

an unnecessary organ for life, was to counterbalance the liver, so that people did not bend to right. It would be 

strange to imagine that an organ, such as the spleen, which weighs approximately 150 grams, would be able to 

counterbalance the largest organ in the body, with four time the spleen weight. Nevertheless, it is important to 

remember the splenomegaly from malaria and schistosomiasis, which were endemic in that period in Egypt and exist 

even today. In these diseases, the hepatic and splenic dimensions are equivalent, and sometimes the size of the 

spleen may be more than double the dimension of the liver. 

Structure of the Spleen [9,10] 

During the Italian Renaissance, Nicholas Massa described the morphology of the spleen in detail, characterizing it as 

a soft and raw sponge, in his book, "Liber Introductorius Anatomiae" (1536). Massa was also the first to correctly 

report on splenic vascularization. 

Unfortunately, Andreas Vesalius, scientist who most contributed to the development of Anatomy, gave little 

importance to the spleen, mentioning in his "De Humani Corporis Fabrica" (1543) only that it was an organ located 

behind the final left ribs and that, in its normal size, it was unpalpable. 

Great advances in splenic morphology are due to Marcelo Malpighi, founder of Microscopic Anatomy. His 

outstanding studies on the spleen, around 1686, resulted in the knowledge of the splenic capsule and its 

intraparenchymatous insertions, in a trabecular form. Actually, the first to write about the splenic capsule was 

Highmore (1651); nevertheless, it received the name of the Malpighi's capsule. 

Comparing the spleen to a fruit, Malpighi called the parenchyma, pulp, and verified the division in two parts which, 

by the colour found in corpses, were called: red pulp and white pulp. According to this anatomist, the white pulp is 

divided into cellular accumulations in the form of curls and received, years later, the name of Malpighi's corpuscles. 

These organelles appear to be glands; however, as they do not possess visible ducts, according to Malpighi, they 

projected “shadows” within the blood circulation. 

Reticular System [16,17] 

Antoine Van Leeuwenhoek (1708), who contributed in the invention of the microscope, also brought important 

morphological knowledge regarding the spleen. He was the first to present details concerning the histology of the organ. 

However, the most well-known microscopic discoveries occurred one century and a half later. Tigri (1847) identified the 

reticular structure of the red pulp of the spleen. A few years later, Albert Christian Theodor Billroth (1857), studying the

20 The Spleen, 2011, 20-36 

Functions of the Spleen and their Evaluation 

Catalin Vasilescu* 



CHAPTER 2 

Fundeni Institute of Digestive Disease and Liver Transplantation, 258 Fundeni Street, Bucharest, Romania 

Abstract: The spleen receives 5% of the total cardiac output every minute and less than 10% of the blood in the 

arterial capillaries is emptied directly in the venous sinuses. It is also a major site for the synthesis of tuftsin and 

properdin, two proteins which serve as opsonins. This organ is the largest lymphoid tissue of the body. Most of 

the splenic functions of fight against pathogens may be taken over by other organs. The major known functions of 

spleen are removal of aging erythrocytes and recycling of iron, elicitation of immunity, and supply of 

erythrocytes after hemorrhagic shock and removes intraerythrocyte inclusions. Up to 30% of platelets are stored 

within the average spleen and can be released in response to specific stimuli such as epinephrine. Splenic function 

can be assessed most simply by searching for Howell-Jolly bodies. The spleen can be visualized and its size 

estimated by scintillation scanning following injection of isotope-labelled, autologous, heat-damaged red cells, 

which are selectively removed by functional splenic tissue. 

Key Words: Spleen, Functions, Phagocytosis, Hematopoesis, Metabolism, Immunology, Filtering. 

SPLENIC FUNCTIONS: AN OVERVIEW 

The spleen receives 5% of the total cardiac output every minute and less than 10% of the blood in the arterial 

capillaries is emptied directly in the venous sinuses. Blood reaches in large amount the splenic red pulp, a filter 

engaged in the removal of particular matter and aged and/or damaged red blood cells [1]. 

Ninety per cent of the blood entering the spleen empties into the “open circulation” of the red pulp, and the blood is 

then forced into the sinuses. This means that the blood cells and other particles contained in the blood are required to 

circulate along the fine meshwork of the splenic cords until they can squeeze through tiny 0.5 to 2.5 μm pores 

between endothelial cells lining the walls of the venous sinuses to enter the venous circulation. This delayed 

microcirculation allows time for splenic phagocytes to remove even poorly opsonized bacteria [2,3]. 

Animal studies with intravenous radiolabelled bacteria showed that the liver can effectively clear the bulk of well 

opsonized bacteria but the spleen is a more efficient filter in removing poorly opsonized bacteria, which are 

predominantly encapsulated organisms. The spleen is also the main site of synthesis of immunoglobulin M (IgM) 

antibody and serum IgM levels fall after splenectomy [2]. 

The spleen is also a major site for synthesis of tuftsin and properdin, two proteins which serve as opsonins. The 

serum levels of tuftsin, a basic tetrapeptide that coats the surface of neutrophils to promote phagocytosis, is 

subnormal after splenectomy [2,3]. 

Removal of the spleen results in decreased serum levels of these factors. Properdin can initiate the alternative 

pathway of complement activation to produce destruction of bacteria as well as foreign and abnormal cells. Tuftsin 

is a tetrapeptide that enhances the phagocytic activity of both polymorphonuclear leukocytes and mononuclear 

phagocytes. The spleen is the major site of cleavage of tuftsin from the heavy chain of IgG, and circulating levels of 

tuftsin are suppressed in asplenic subjects. 

The spleen is the largest lymphoid tissue of the body. The white pulp represents the immunological compartment of 

the organ with both antigens and lymphocytes and is divided into B and T lymphocyte zones [1]. 

*Address correspondence to Catalin Vasilescu: Fundeni Institute of Digestive Disease and Liver Transplantation, 258 Fundeni Street, 

Bucharest, Romania; E-mail: catvasilescu@gmail.com

Functions of the Spleen and their Evaluation The Spleen 21 

In humans, memory B cells constitute 30 – 60% of all B cells and are recognized by surface expression of CD27. Half 

of them are IgM B memory cells and the rest are switched class memory B cells. Memory B cells persist in the 

individual, rapidly produce antibodies upon a second challenge with the same pathogen. IgM memory B cells are 

characterized by few somatic mutations in comparison to switched class memory B cells, which have highly mutated 

VH sequences. The spleen appears to be indispensable for the survival of IgM memory B cells; it is not clear if the 

spleen is the site of generation of these cells or is producing an environment that supports their survival. IgM memory 

B cells produce natural antibodies and are necessary for T-independent responses against encapsulated bacteria [2]. 

Most of the splenic functions of fight against pathogens may be taken over by other organs. The defense against 

encapsulated bacteria cannot be replaced because the spleen is a crucial site of early exposure to that antigens [4]. 

Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis are a constant threat to 

splenectomized patients. 

Patients who are asplenic, either because of physical absence of a spleen or functional splenic compromise, are at an 

increased risk of contracting a overwhelming postsplenectomy infection (OPSI). This condition is commonly 

described as a fulminant bacteremia that develops very quickly and carries a high mortality rate. The incidence of 

OPSI has been difficult to establish, partially because of the wide variation in occurrence rates among particular 

groups of patients. In one population-based study, the incidence of OPSI in splenectomy patients was found to be 

0.23%. However, other studies have demonstrated rates of serious bacterial infection as high as 21% to 22% in 

patients with specific medical conditions, such as thalassemia major or hematologic malignancy. For most patients, 

the risk of sepsis is substantially increased in the first 2 to 3 years following splenectomy. However, patients have 

developed life-threatening infection as many as 10 years after their surgery. The lifetime risk of OPSI has been 

estimated at 5%. 

While the risk of contracting OPSI may be low in some populations, once an infection occurs, the mortality rates are 

high, ranging from 38% to 69%, and fulminant infections frequently develop in patients who are relatively young 

and have few other health problems. Early diagnosis and intervention are the keys to a good outcome [5]. 

Two splenic functions are decisive for the defense against infections by encapsulated bacteria and for OPSI 

prevention: 

antibodies production against LPS. 

phagocytosis of opsonized particles in the so-called opencirculation of the splenic red pulp cords [6]. 

There are also numerous physiological minor differences between mammals. The reservoir of red blood cells in the 

spleen differs dramatically between some species. Megakaryocytes are numerous in the mouse, but not the human, 

spleen [7]. 

A SHORT NOTE ON SPLENIC STRUCTURE WITH DETAILS ON MORPHOLOGICAL DIFFERENCES 

BETWEEN MAN AND RODENTS. 

The spleen histology and histopathology are presented elsewhere in the book. However, most of the knowledge we 

have at present on splenic functions are based on experimental data and/or on morphological studies obtained in 

different laboratory animals, especially mice and rats. Some recent publications are emphasizing the significant 

differences between the spleen morphology in humans and other non-primate species, differences that may be 

crucial for the understanding of the main splenic functions. 

Therefore, we consider it would be a good start point in the discussion of splenic functions to clarify this aspect. The 

following description is mainly based on the recent reviews of structure and function of the spleen discussing some 

elegant data on microscopic anatomy in humans and rodents [6,4]. 

The complexity of the spleen’s anatomical architecture is achieved during development through intricate interactions 

and signals between spleen mesenchymal cells and invading endothelial and hematopoietic cells. However, little is

22 The Spleen Catalin Vasilescu 

known about how the precise spatiotemporal organization of these events gives rise to the sophisticated microarchitecture 

of the developing spleen [7]. 

An organ such as the spleen has several histologically defined regions. On the largest scale are the red and white 

pulps, areas which define the predominantly erythroid and lymphoid areas respectively. Within the white pulp three 

additional areas are readily discernible even to the gifted amateur: these areas are the marginal zone (MZ); the 

periarteriolar lymphoid sheath (PALS); and the follicle. Each of these areas has particular characteristics important 

for its function in the immune system. 

The MZ is the site of lymphocyte entry into the spleen from the blood and is home to specialized macrophages plus 

an IgMhilgDIo B cell subset. The PALS is the T cell area and is also rich in a specialized antigen-presenting cell 

type called the interdigitating dendritic cell. The follicle is the B cell area of the white pulp and contains, in addition 

to B cells, follicular dendritic cells (FDCs) which function as efficient antigen-capture cells [8]. 

Morphology of the Splenic Marginal Zone in Mice And Rats 

In rodents two B cell compartments exist in the spleen: the follicles and the MZ. 

- Follicles - contain small recirculating B lymphocytes, which co-express surface IgM and IgD. In 

secondary follicles these B cells are located to the periphery and form the mantle zone or corona. 

- The MZ - surrounds the entire surface of the white pulp. At the inner border of the MZ are situated the 

marginal sinus and the marginal metallophilic macrophages. Within the MZ another macrophage 

population may be distinguished, the MZ macrophages, cells with well established 

immunohistological caracteristics. For information on immunohistology see Steiniger 2006 [6]. 

The MZ is also colonized by immature dendritic cells from the blood heading for the T cell zone. The rodent MZ 

appears to be an open compartment because besides migratory lymphocytes and dendritic cells, particulate materials 

and entire encapsulated bacteria end up in this region after intravenous injection. Encapsulated bacteria are then 

phagocytosed by MZ macrophages and lead to IgM antibody responses. Stromal cells are clearly present in the MZ, 

but their phenotype is unknown [6]. 

Morphology of the Splenic Marginal Zone in Humans 

Several immunohistological studies have indicated that a marginal sinus and marginal metallophilic macrophages do 

not exist in humans [6]. Thus, there is no inner border of the MZ equivalent towards the mantle zone or the primary 

follicles. Although macrophages are present in the human MZ equivalent, these cells do not exhibit any special 

phenotype distinct from that of red pulp macrophages. 

Human MZ B cells appear to reside only in a superfficial follicular compartment and do not extend along the T cell 

zone. The human splenic follicles exhibit two particularities absent in rodents: 

- The arrangement of CD27+ cells at a variable superfficial compartment in human splenic and extrasplenic 

follicles. In humans, but not in mice or rats, the expression of CD27+, a member of the TNFreceptor 

family, is closely associated with the expression of hypermutated variable regions of surface 

Ig in B cells. Thus, CD27 has been suggested as an indicator of memory cell diVerentiation in human 

B cells. 

- An extension of the T cell zone surrounds human splenic follicles within the marginal zone 

equivalent. These extension of the T cell zone at the surface of the follicles, which appears to divide 

the MZ equivalent into an inner IgD +/ - CD27+ area and an outer IgD + CD27 +/- region [6]. 

The special fibroblasts of the T cell region continue around the follicles. These fibroblasts correspond to the 

“fibroblastic reticulum cells” mentioned in older publications and exhibit a unique morphology and phenotype. 

The most interesting of the molecules detected on the fibroblasts extending at the follicular surface is clearly 

MAdCAM-1, because this molecule has not been described in fibroblasts outside the spleen in humans.

Histology and Histopathology of the Spleen 

Kim Vaiphei* 

Department of Histopathology, PGIMER Chandigarh India 

The Spleen, 2011, 37-74 37 



CHAPTER 3 

Abstract: Specimen of a spleen is most frequently encountered in centers that deal with autopsy cases. Spleen is 

not a frequent surgically resected specimen thereby indicating its uncommon presentation with a primary 

disorder. Most pathologists tend to have a casual approach or consider spleen to be an organ with a difficult or a 

non-specific morphology. Understanding and interpreting splenic pathology remain a challenge for a pathologist. 

There are only few diseases which primarily involve the spleen and represent involvement by diseases originating 

elsewhere. The contribution of a histopathologist in such situation is in confirmation of the clinical diagnosis or 

exclusion of a suspected pathology. Splenic pathology is of a combined interest to a surgeon, hematologist, 

histopathologist and an oncologist. There are certain prerequisites for a proper interpretation of splenic pathology 

like availability of an adequate clinical history, lab investigation, systematic gross examination and studying of 

sections from a properly fixed specimen. A freshly removed specimen of spleen needs to be thoroughly examined 

after removal of the attached fat, lymph nodes; splenicule if any and other undesired adherent tissue on the 

capsule and the hilum. Vessels at hilum are left with adequate length for examination and detail study if need be. 

After cleaning, the spleen is weighed and measured. The specimen is cut with a sharp knife at an interval of 5 mm 

thickness along the length exposing the hilum. Any excess blood is shocked with a clean towel and smears can be 

made. Alternatively, excess blood can be cleaned by washing gently under running tap water. The cut slices are 

put into fixative and left overnight for fixation. The smears can either be fixed immediately with absolute alcohol 

or left to dry in the air. Representative sampling can be done immediately in the fresh state or after overnight 

fixation. Number of blocks to be sampled will depend on the size and gross feature of the specimen. Minimum of 

two blocks is usually sampled from different area of the spleen including the hilum and capsule. 

PARTIAL SPLENECTOMY AND SPLENIC BIOPSY 

Clinical use of total splenectomy in children is restricted by the concern of overwhelming post-splenectomy sepsis 

which may increase by 60 to 100 folds compared to children who have not had splenectomy. Risk of overwhelming 

post-splenectomy sepsis is reduced by immunization against Streptococcus pneumoniae, Meningococcus, 

Haemophilus influenzae and postoperative antibiotic prophylaxis. Its risk is never completely eliminated and the 

concern of incomplete protection persists [1-3]. Partial splenectomy has been tried as an alternative to total 

splenectomy with the goal of removing enough spleen to gain the desired hematologic effect while preserving the 

splenic immune function. However the practice of partial splenectomy is of limited use because of the technical 

difficulties, bleeding associated with the surgical procedure and the possible splenic regrowth [4-6]. Similarly, a trucut 

biopsy of the spleen that can assist in the diagnosis of hematological malignancies is not usually performed due 

to the associated complications as in partial splenectomy [7,8]. More recently with the availability of radiofrequency 

generated heat, virtually a bloodless partial splenectomy and biopsy of the spleen could be carried out successfully. 

Fine-needle aspiration (FNA) biopsy is a modality that can be of help in establishing the diagnosis of focal splenic 

lesion. Complications associated with FNA have been documented in up-to 12.5% [9-11]. These techniques are 

better practiced under ultrasonographic guidance for a more appropriate sampling. Guided FNA biopsy is reported 

to have 97.8%–100% diagnostic yields [11]. 

Splenic pathology is classifiable under various categories. It can be grouped into i) splenic disorder in systemic 

disorder which is seen more commonly than ii) the primary splenic disorder. To simplify the various disorders, 

enlargement of the spleen can be diffuse or focal. Almost any bacterial or viral infection will cause diffuse splenic 

enlargement. In a diffusely enlarged spleen, changes in the splenic parenchyma will dominantly involve the white 

pulp as in septicemia, lymphoid hyperplasia and lymphoma infiltration. Diffuse expansion of the red pulp is seen 

when there is diffuse infiltration by extramedullary hematopoietic cells, sinusoidal histiocytic proliferation, 

*Address correspondence to Kim Vaiphei: Department of Histopathology, PGIMER Chandigarh India; kvaiphei2009@googlemail.com

38 The Spleen Kim Vaiphei 

leukemic cells (acute and chronic), hairy cell leukemia and lymphomas. Spleen can be focally involved by 

inflammatory conditions of any etiology, acquired or congenital cystic lesions, pseudo tumor, and benign and 

malignant tumors. 

SPLENITIS 

The literal meaning of splenitis is inflammation of the spleen. It is a condition manifested by mild to moderate 

enlargement of the spleen associated with local pain. It is usually observed in autopsy specimen as a patient’s spleen 

is not surgically removed to diagnose a systemic infection or septicemia. Main types of splenitis are: i) purulent 

splenitis caused by hematogenous bacterial spread, ii) granulomatous splenitis as the result of infection by certain 

bacteria such as necrobacillosis, tuberculosis, pseudotuberculosis as well as fungi and iii) hyperplastic splenitis 

caused by virus and protozoa. 

Purulent Splenitis Seen in Bacterial Septicemia [12-15] 

A patient who is terminally ill acquires respiratory tract infection in the hospital or from the community tends to 

develop a full blown septicemia. Patients admitted in the hospital are invariably treated with broad spectrum 

antibiotics, the respond can be variable and some of them may die of the septicemia. Anatomic finding of the spleen 

in sepsis is non-specific, limiting to a soft and mushy spleen called as septic splenitis which has been referred as 

nonspecific acute splenitis. A septicemic spleen is an enlarged, soft, congested and diffluent (very soft and runny), 

sometimes with infarcts (Fig. 1). Microscopically, there is presence of neutrophils in both red and white pulps (Fig. 

2). There can be microscopic foci of necrosis and lymphoid tissue depletion (Fig. 3). A patient who had been treated 

with antibiotics, the enlarged and soft spleen may show lack of infiltration by neutrophils, depleted white pulp and 

congested red pulp. A chronically ill anemic patient may have evidence of extramedullary hemopoiesis in the red 

pulp. These non-specific changes observed in the spleen is the result of the microbiologic agents and the cytokines 

released by the systemic immune stimulation. Earliest inflammatory response following experimental injection of 

endotoxin and bacterial antigen had been studied in cryosection of spleen. Neutrophils were observed to appear by 

90 minutes at white and red pulp junction and neutrophils were also observed migrating to T cell area in 10-12 hours 

time along with the appearance of the macrophages in germinal centers [16]. Overwhelming infection can result in 

destruction of lymphocytes in the follicular center producing lympholysis and lymphoid depletion, epithelioid 

germinal center and intra-follicular hyalinosis. A purulent splenitis can also be the result of hematogenous bacterial 

spread from thromboembolic endocarditis and abscesses. In subacute form of splenitis, there is macrophage 

proliferation in the sinuses and lymphoid follicular hyperplasia in the white pulp (Fig. 4). Spleen can be the 

dominant organ involved in hemophagocytosis syndrome of infection associated or familial type [16-20]. The spleen 

is mildly enlarged with no characteristic gross feature. Microscopy will show expansion of the red pulp and 

depletion of the white pulp with marked proliferation of the macrophages showing hemophagocytosis indicated by 

the presence of intracytoplasmic RBC and lymphocytes (Fig. 5). The phagocytosed cells are seen well in Masson’s 

trichrome staining where RBC stains red. In viral associated hemophagocytosis, there is hyperplasia of the lymphoid 

follicles with prominent germinal center. The reticuloendothelial cells present within these reactive follicles can also 

reveal hemophagocytosis. 

Figure 1: Gross photograph of capsular aspect of a grossly enlarged spleen from a patient who died with uncontrolled 

septicemia. The capsule shows fibrinous exudates and multiple dark discoloured areas of fresh infarcts. As there is marked 

parenchymal congestion, the capsule shows dimpling effect.

Histology and Histopathology of the Spleen The Spleen 39 

Figure 2: Microphotograph to show splenic sinuses packed with neutrophils. (HE,x540). 

Figure 3: Low power photomicrograph to show lymphoid depletion and sinusoidal congestion in a partially treated case of 

septicemia. (HE,x50). 

Figure 4: Low power photomicrograph showing reactive lymphoid follicle and prominence of macrophage in splenic sinuses. 

(HE,x150). 

Figure 5: High photomicrograph showing active haemphagocytosis by an activated macrophage within splenic sinus. (HE,x750).

Some Aspects of Splenic Pathology 

Alfredo J. A. Barbosa* 

The Spleen, 2011, 75-83 75 

School of Medicine, Federal University of Minas Gerais, Belo Horizonte, M.G., Brazil 



CHAPTER 4 

Abstract: The spleen is the largest lymphoid organ in the body. It is located in the left hypochondrium and is 

surrounded by a thick, fibrous capsule that adheres to the parenchyma. In human beings the spleen has an 

elongated shape and weighs 100-200 grams, with its major diameters measuring 11 x 7 cm. It receives blood 

mainly through the splenic artery, derived from the celiac trunk, and venous drainage is processed through the 

splenic vein that leads into the portal vein. When studying the pathologic anatomy of the spleen one should keep 

in mind the lymphoid and the vascular nature of the organ as well as its shape, size and weight. As we shall see, 

in most cases the gross anatomy of the spleen is directly or indirectly associated with local and systemic vascular 

and hemodynamic changes and also with changes of haematolymphopoiesis. Changes in these different systems 

frequently manifest as modifications of the weight and volume of the spleen. 

Several functions are performed by the spleen, each one correlated with a specific anatomic site in the organ. 

Most of these functions are usually complementary to those of other organs and thus are not always important in 

normal adult individuals, but can acquire importance in disease states. The better known functions of the spleen 

are haematopoiesis, acting as a reservoir of blood elements (mainly platelets), phagocytosis (removal of altered 

blood cells and other particulate matter), and several roles in the immunologic mechanisms. 

Histologically, the spleen can be divided into two distinct regions, i.e., the white pulp and red pulp. These two 

regions are separated by an ill-defined interphase known as the marginal zone. The white pulp is made up of T 

and B lymphocytes, the former located along the periarteriolar lymphoid sheath and the latter in the lymphoid 

follicles, while the red pulp consists of a network of venous sinuses and the Billroth’s cords. The Billroth’s cords 

contain numerous macrophages which are responsible for the important phagocytic function of the organ. The 

sinuses are lined with a particular type of endothelial cells forming a discontinuous barrier which allows passage 

of blood cells between cords and sinuses. 

CONGENITAL ANOMALIES 

Asplenia is the congenital absence of the spleen. Like hypoplasia, it seems to be a rare anomaly. This condition is 

frequently associated with heart malformations. Other congenital anomalies of blood vessels, lung and abdominal 

viscera can also be found in these cases. The occurrence of a hereditary form of spleen hypoplasia has been reported. 

[1] Abnormal grooves on the surface of the spleen giving a lobulated aspect to the organ are not infrequent. An 

accessory spleen, also called supernumerary spleen, is frequently observed. It may be a single or multiple structure, 

usually spherical, small, and most frequently localized in the gastrosplenic ligament or in the tail of the pancreas. 

These small ectopic spleens may occupy unusual locations, being intimately close to the pancreatic parenchyma or 

presenting complete or incomplete fusion with gonadal, usually testicular, mesonephric structures. Cases of 

splenohepatic and splenorenal fusion have also been reported. Not infrequently, these ectopic spleens can mimic 

neoplasm lesions in the pancreas or adrenals [2,3]. They usually present the same histological structures as the 

normally located organ and can also respond to the same stimuli, a fact that explains their clinical importance. 

CYSTS OF THE SPLEEN 

Primary epithelial cysts (epidermoid cysts) and parasitic cysts are the main types of cysts that have been reported in 

the human spleen. Primary epithelial cysts usually are solitary, mainly seen in children, and can be present also in 

accessory spleens [4]. Trabeculation is frequently found on their inner surface and, microscopically, their wall is 

lined with cuboidal cells, mesothelial-like cells or squamous epithelium. When squamous epithelium is present they 

are frequently named “epidermoid cysts”, even in the absence of skin adnexa. They are believed to be of 

teratomatous origin or to originate from fetal squamous epithelium or mesothelial cells [1] . Most epithelial splenic 

cysts are large and splenectomy may be the first option of medical treatment (Fig. 1). Although infrequent, 

*Address correspondence to Alfredo Jose Afonso Barbosa: Professor of the Department of Pathology, School of Medicine, Federal 

University of Minas Gerais, Belo Horizonte, Brazil

76 The Spleen Alfredo J. A. Barbosa 

secondary epithelial cysts, usually derived from mucinous tumours at different sites, can be found in the spleen; 

among them are the mucinous epithelial cysts as components of the pseudomyxoma peritonei. In addition to 

epithelial cysts, the so-called pseudocysts have been detected in the spleen, most of them derived from trauma, 

usually solitary and asymptomatic, as well as the parasitic cysts resulting from Echinococcus infestation. 

Figure 1: Gross appearance of a large epithelial splenic cyst. 

CONGESTIVE SPLENOMEGALY 

Regardless of its origin, persistent or chronic venous congestion causes changes in the spleen known as "congestive 

splenomegaly" or "fibrocongestive splenomegaly”. Grossly, the main changes are a variable, sometimes severe 

enlargement of the organ, associated with a corresponding increase of its weight. Thus, the organ becomes large, 

firm and dark (Fig. 2). Obstruction of venous drainage within the splenic vein and portal hypertension are the most 

important causes and are responsible for higher rates of increase in spleen volume. The spleen frequently reaches 

1,000 grams in weight, and cases of congestive splenomegaly reaching a weight of 3,000-4,000 grams are not 

uncommon. The main histopathologic changes of congestive splenomegaly are the marked dilatation of the veins 

and sinuses, fibrosis of the red pulp and the presence of numerous hemosiderin-containing macrophages. Diffuse 

collagen fibrosis of the red pulp may be of variable intensity and is partly responsible for the increased weight and 

volume of the organ and for the name "fibrocongestive splenomegaly”. Areas of recent haemorrhage are frequent. 

The Gandy-Gamma corpuscles are frequently found in the most severe cases. They are focal lesion formed by areas 

of fibrosis associated with deposits of calcium salts (Fig. 3). The Gandy-Gamna corpuscles can be seen with the 

naked eye as small grayish nodules scattered along the spleen cut surface. 

Cirrhosis is by far the most common worldwide cause of portal hypertension and congestive splenomegaly. In countries, 

or in regions, where schistosomiasis (S. mansoni) is endemic, the so-called “hepatosplenic form” of this parasitic disease 

is also an important cause of portal hypertension associated with often severe congestive splenomegaly. Other causes of 

portal hypertension are thrombosis of hepatic veins (Budd-Chiari syndrome), thrombosis of the splenic veins, and 

recanalized splenic vein thrombosis, also called “cavernous transformation”. Portal vein thrombosis may be the result of 

inflammation (phlebitis), trauma or neoplasm infiltration. These cases of severe congestive splenomegaly may be 

accompanied by signs of hypersplenism such as anemia, leucopenia and thrombocytopenia. 

In addition, congestive splenomegaly may be due to heart failure involving the right heart and, therefore, can be 

found in those subjects with long-term congestive heart failure or cor pulmonale. During the course of heart failure, 

congestive splenomegaly is just a secondary element of the generalized visceral congestion. Unlike the cases of 

portal hypertension, which produce conspicuous increases in the size of the spleen, i.e., congestive splenomegaly 

associated with congestion of central origin, the splenomegaly is only slight or moderate, and the spleen rarely 

exceeds 300-400 grams in weight.

Some Aspects of Splenic Pathology The Spleen 77 

The main physiopathologic reaction of the spleen in splenomegaly conditions is generically called hypersplenism. 

This denomination indicates increased functions such as blood cell sequestration and destruction, immune function 

and production of lympho-haematopoietic elements. Hypersplenism has no specific morphological presentation, but 

can coexist with tissue changes indicative or consistent with clinically observed pathophysiological changes. Thus, 

cytopenia and splenomegaly are considered to be components of hypersplenism, and the retest is the reversal of the 

clinical picture after splenectomy. The cases of hypersplenism associated with volumetric enlargement of the spleen 

are mostly attributed to changes in the red pulp with increased filtering mechanisms. In other cases, the increased 

destruction of blood cells results from related defects, as is the case for spherocytosis. There are no known specific 

microscopic changes that may characterize hypersplenism. 

Figure 2: Gross view of the cut surface of the sclerocongestive spleen. The spleen is large and firm. Fibrous thickening of the 

capsule can be easily seen. 

Figure 3: Microscopic appearance of a Gandy-Gamna corpuscle frequently present in sclerocongestive splenomegaly. 

SPLENIC INFARCTION 

Infarction of the spleen is relatively common and may result from thrombosis of the splenic vein or its major 

tributary branches. It can also occur in association with massive fibrosplenomegaly. Infarction can occur as a single 

lesion or as multiple ones, most of them of the “anemic” type, also called “white infarctions”. These lesions present 

a typical wedge-shaped gross pattern, with the base toward the capsule. At other times, their anatomical outline is 

more irregular in appearance, resembling a geographical map; in these cases they are usually due to obstruction of

84 The Spleen, 2011, 84-116 

Sepsis and the Spleen 


Department of General Surgery, Medical School, Rio de Janeiro State University, Rio de Janeiro, Brazil 



CHAPTER 5 

Abstract: Since ancient times, the spleen is regarded as a mysterious and intriguing organ. It has various 

functions underscoring its prepoderant relevance as the largest secondary lymphoid organ system. Total 

splenectomy done at any age and for any reason increases the risk of death from overwhelming postsplenectomy 

infection (OPSI). The etiologic agents most frequently found in OPSI are Streptococcus pneumoniae, 

Haemophilus influenzae type B, and Neisseria meningitidis, but other bacteria such β-hemolytic Streptococcus, 

Staphylococcus aureus, and Escherichia coli, Pseudomonas sp., also present a significant risk. Prophylaxis of 

OPSI is located in three main categories: patient education, immunoprophylaxis, and chemoprophylaxis. Besides 

these, the realization of heterotopic splenic autotransplantation after splenectomy seems to favor the recovery of 

some of the functions of the spleen. However, these measures seem to be not sufficient to prevent the higher risk 

of developing OPSI. Because of this risk, the indication for the realization of total splenectomy in trauma and 

several diseases has been sharply declining. The objective of this work is to make a description of the aspects that 

correlate the absence of spleen with the occurrence of sepsis. 

Key Words: Overwhelming postsplenectomy infection. Spleen. Splenectomy. Prophylaxis. Splenic auto-implant. Sepsis. 

INTRODUCTION 

The term “spleen” derives from the Greek word σπλήν (splén), which seems to arise from σπλαϒΧνον (splanchnon – 

viscous, viscus) or σπάω (to spawn – remove). The origin of these words allows the assumption that the ancient 

Greeks had already identified the spleen as a viscous body which removed impurities from the blood. By removing 

"sp" from splén, we have the term “lien”, the Roman name for the spleen. In Sanskrit, the oldest Indo-European 

language, its name was plihan or plihaa [1]. 

HISTORY 

Since the ancient times of the history of civilization, the spleen was recognized as 'a mysterious organ,' with doubts 

existing about the importance of its function. Indeed, Aristotle, around 350 BC, stated that it was not necessary for 

life. During the first century, the Roman historian Plinius endorsed its removal in racing athletes, believing that they 

would run more quickly without the organ, but he warned that these athletes would lose 'the ability of laughter and 

happiness', a statement also later detected in the Babylonian Talmud [1].These are some of the understandings that 

existed about the spleen more than 2,000 years ago. Since then, famous scholars and physicians, such as Claudius 

Galenus, Andreas Vesalius, William Harvey, Marcello Malpighi, Jules Péan, Theodor Billroth, Samuel Gross, 

William Mayo, and Marcelo Campos Christo inquired about the physiology and importance of this organ and, more 

recently, began to propose alternatives to its resection [1, 2]. 

During most of that time, it was believed that splenic excision would not lead to any harmful consequences to the 

patients. Although the surgical removal of the spleen may have occurred since ancient times, the first known record 

of a total splenectomy concerned the operation performed by Adriano Zaccarelli in 1549, in Naples, Italy, in a 24year-old 

patient with "obstructed spleen”, probably due to malaria [1]. 

With regard to abdominal trauma, the record of surgical procedures involving the spleen is curious, considering that, 

in 1590, Francisco Rossetti performed the first partial splenectomy, while the first total excision of the organ for the 

same indication was only reported by Nicholas Mathias in 1678 in Cape Town, South Africa. It is also interesting to 

*Address correspondence to Ruy Garcia Marques: Department of General Surgery, Medical School, Rio de Janeiro State University, Rio de 

Janeiro, Brazil; E-mail: Rmarques@uerj.br

Sepsis and the Spleen The Spleen 85 

note that of the first ten splenectomies reported in the literature, regardless of indication, at least four, and perhaps 

five, were partial splenectomies. R. L. James, in the United States, was the first to successfully perform a 

splenorrhaphy in 1892, a transfixing suture of the spleen due to a firearm wound [1,3]. 

Especially since the introduction of anesthesia in the 19th century, total splenectomy has been commonly practiced 

in cases of abdominal trauma or injuries resulting from handling during surgical procedures in the upper abdomen, 

even if the organ presented minimal lacerations [4-27]. The resection of the entire splenic mass was also commonly 

practiced until recently in many elective situations for therapeutic or diagnostic purposes, in hematologic, oncologic, 

metabolic, and immunologic disorders, as well as in portal hypertension and in many splenic diseases, such as 

tumors and abscesses [6,11,19-21,28,29-36]. It was only since the mid-twentieth century that we began to have the 

notion that the spleen was relevant by performing multiple functions, especially regarding the immune response. 

Claudius Galenus (130-200 AD), reinforcing the idea then prevailing that the spleen had a digestive function, 

described the communication between it and the stomach by means of vessels (Galen’s ducts), which in reality are 

the splenogastric vessels between the gastric fundus and the upper splenic pole. At that time, Galenus’ knowledge of 

anatomy was the most advanced, considering that he had practiced many dissections of animals and, as a doctor of 

the gladiators of Rome, had also operated on a large number of wounded soldiers. His teachings were obeyed for 

almost 15 centuries, only being strongly contested by Andreas Vesalius (1514-1567) who, in 1543, opposed his 

authority and corrected many of his anatomical misunderstandings. Vesalius noted that the vascularizations of liver 

and spleen differed significantly, but unfortunately rejected the similarities between these two organs. Although 

Vesalius had not made a great contribution to the study of the spleen, the correction of some errors of Galenus, 

besides his great contribution to the development of Anatomy, qualify him as one of the leading figures in the 

history of Medicine [1]. It was William Harvey (1578-1657) who, in 1616, first described the blood circulation, thus 

being able to contest the claim of Galenus in two important aspects: that the venous and arterial systems were 

independent and did not communicate, and that the blood of the spleen was taken by the splenic vein, and not the 

inverse [1,37-40]. 

Marcello Malpighi (1628-1694), the founder of Microscopic Anatomy, described the capsule of the spleen 

(Malpighian capsule) and possibly was a pioneer in observing the input of blood through separate vessels within its 

parenchyma, raising the first considerations about the splenic segments. Using dissection of human cadavers, he 

described the splenic parenchyma as a pulp which featured cellular accumulations in the form of clusters, known as 

the Malpighian corpuscles and was divided into two parts: the red pulp and the white pulp [2]. 

Jules Péan (1830-1898) reported the completion of the first successful elective splenectomy in the 19th century, a 

segmental resection. Considering the arrangement of the arterial system of the spleen, which goes toward 

independent segments, he performed successive sutures of the various branches of the splenic artery, resulting in the 

isolation of a part of the spleen where there was a cyst. With that procedure, Péan started to lay the technical 

foundations for partial splenic resection [2,41]. 

In 1857, Theodor Billroth (1829-1894), studying the reticular structure of the red pulp of the spleen, discovered the 

capillary sinusoids, as well as cellular cords located between the venous sinuses (splenic cords of Billroth). It was 

Billroth who, in 1881, detected a scar in the spleen during an autopsy. He considered it to be a consequence of a 

spontaneously healed old injury, an observation that would allow the possibility of conservative treatment of splenic 

trauma [2,42]. Samuel Gross (1805-1884), in 1882, suggested the basics for the conservative treatment of splenic 

trauma: rest with a light diet in cases of minor bleeding, and lead acetate, opium, and ergot, in most cases of more 

severe bleeding [2]. 

William Mayo (1861-1939), in 1910, successfully performed three partial splenic resections: one due to trauma, one 

due to a twisted splenic pedicle, and the third for the treatment of an abscess in the upper pole of the spleen. Based 

on the good outcome of these patients, he advocated that the spleen should be preserved whenever possible. In that 

same year, Mayo also performed a splenorrhaphy in a patient with a firearm wound [3,43]. 

In 1962, Marcelo Barroca Campos Christo (1920 -), in Belo Horizonte, MG, Brazil, based on studies of anatomical 

specimens, reissuing and improving the contributions of Péan in the mid-nineteenth century, and on studies 

conducted by Antonio Zappalá in 1958 and 1959, reported the results of his evaluation of the technique of partial

86 The Spleen Ruy Garcia Marques 

splenectomy. Of the eight patients with abdominal trauma in which he performed splenic segmental resection, seven 

survived (another patient also died after 30 days due to gastric perforation). The monitoring of the six survivors 

showed no complications, which led to the assumption that systematized partial splenectomy could be adapted to 

any traumatic injury of the spleen limited to a defined vascular segment. Campos Christo's work remains one of the 

most cited in the world in the discussion of the conservative approach to splenic surgery [2,44-46]. 

Infection in the Absence of the Spleen 

Since the 18 th century, rapidly fatal infections have been reported in patients who had undergone total resection of 

the spleen. Johannus Ferrerius, in 1716, reported that he performed a successful total splenectomy in 1711 to treat a 

splenomegaly due to malaria in a 30-year-old patient. Five years after the procedure, the patient developed 

erysipelas, rapidly progressing to generalized infection and death. (apud Petroianu, 2007) [35]. However, it was only 

in the late 19 th century that the first correlations between sepsis and splenectomy began to be suggested. 

In 1883, Tizzoni & Cattani (apud Morris & Bulock) inoculated three groups of rabbits with cultures of the tetanus 

bacillus. Both vaccinated and non-splenectomized animals resisted inoculation, while those vaccinated 15 days after 

splenectomy died at roughly the same time as non-vaccinated rabbits [47]. A few years later, in 1891, Bardach (apud 

Morris & Bullock) conducted two experiments that have become classics in the description of the subject: he 

injected an anthrax culture into the abdominal cavity of 25 dogs subjected to total splenectomy and into the 

abdominal cavity of 25 healthy dogs, with death occurring in 19 dogs of the first group and in only five of the 

second group. In a second experiment, he immunized rabbits with attenuated cultures of anthrax; of 35 

splenectomized animals, 26 died, while intact control animals showed a much lower mortality rate [47]. 

A. B. Luckhardt & F. C. Becht, in 1911, compared the production of hemolysins, hemagglutinins, and animalspecific 

hemopsonins between non-splenectomized and splenectomized animals and noted that those with an intact 

spleen were more efficient in producing these 'immune bodies' [48]. 

In 1919, Morris & Bullock showed that total splenectomy might result in increased susceptibility to infections in rats 

and that asplenic animals were less able to control bacterial sepsis. These authors injected a culture of Bacillus 

enteritidis into the abdomen of 36 splenectomized rats, with death occurring in 80.5% of cases, whereas only 38.9% 

of intact control rats died [47]. 

F. J. O'Donnell was the first to suggest, in 1929, the correlation between total splenectomy in humans and a 

reduction of the body's natural resistance to infection. He reported the case of a six-year-old child who underwent 

total splenectomy for Banti's disease in its early stages and who died two years later due to fulminant sepsis. 

O'Donnell also stated that the father of this child, also splenectomized, had died a few years after the procedure due 

to acute pulmonary sepsis [49]. During O’Donnell’s report at a scientific meeting, G. E. Nesbitt proposed that it 

would be valuable to collect data about the survival of all patients who had undergone total splenectomy, [49]. 

starting to spread the possibility of a strong association between sepsis and asplenic individuals. 

In 1952, King & Shumacker reported severe infectious complications after total splenectomy due to congenital 

hemolytic disease in five children under six months of age. Four of these children developed clinical signs of 

meningitis or fulminant meningococcemia between six weeks and three years after surgery, and one died. The fifth 

child developed an unknown and quickly fatal febrile illness a few days after being discharged [50]. The description 

of King & Shumacker Jr constitutes a landkmark in the literature regarding the evidence of an association between 

splenectomy and sepsis. Nevertheless, initially it was thought that the risk would be limited to children. 

Elliot F. Elis & Richard T. Smith, in 1966, published a review of the immunological properties of the spleen recognized 

at the time, arguing that the organ was able to quickly and effectively mobilize an immune response specific to some 

microorganisms in the bloodstream, such as pneumococci. These authors concluded that the synthesis of specific 

antibodies was initiated within splenic capillaries, where phagocytosis could efficiently occur [2,51]. 

Louis Diamond, in 1969, drew attention to what he called overwhelming postsplenectomy infection (OPSI), a 

clinical entity distinct from other types of sepsis or bacteremia present in individuals with a preserved spleen,

Surgical Anatomy of the Spleen 


The Spleen, 2011, 117-133 117 




CHAPTER 6 

Abstract [1-4]: Although known for more than 3,000 years, the spleen continues to be one of the most 

misunderstood human organs, even from a morphological point of view. Its disregard among the majority of 

doctors and researchers is responsible for the sparse and discontinued anatomical studies regarding the spleen. 

The major consequence resulting from the indifference of the scientific and medical worlds towards this organ 

has occurred in surgery, considering that spleen operations have progressed during the last twenty years more 

than throughout the history of Medicine. It is not fair to realize that the dogma that still predominates amongst 

doctors is that spleen surgery results simply in “through out the spleen!”. 

This demonstration of medical ignorance and the lack of professional sensibility trend to be modified by the 

scientific works of recent decades. Discoveries regarding the functioning of the spleen have aided a number of 

anatomy specialists in improving their efforts regarding the morphology of the spleen. The foundations of these 

scientific advances have affected new surgical proposals for this organ and its vascular pedicle. The benefits of 

new surgical proposals have increased the survival rate among many patients as well as reduced the complications 

that the “spleen removers” once imposed upon their victims. 

Key Words: Anatomy, Spleen, Splenectomy, Morphology, Artery, Vein, Nerve, Lymphatic, Surgery. 

EMBRYOLOGIC ASPECTS [4-12] 

The spleen originates from the dorsal mesogastrium, beginning with the mesenchymal cells, which differentiate 

themselves as of the fifth embryonic week. Such cells are brought to this region by the mesenchymal tissue, which 

later forms the splenic vessels. 

The 90 o rotation of the primitive stomach, in the sixth week of embryonic life, displaces the multiple spleen cell 

accumulations from the dorsal median to the left subdiaphragmatic site. 

In the eighth week, vasculogenesis occurs, together with the constitution and integration of blood vessels from the 

pedicle and the parenchyma. In the thirteenth week, the formation of B and T lymphocytes begins, as does the 

production of immunoglobins. Upon entering the fourth month of life, the foetus presents the spleen as a 

conglomeration of blood vessels surrounded by fusiform cells which form a haematopoetic pulp. In this manner, the 

spleen and liver become the first blood producing organs. 

In the sixth month, the red and white pulps become clearly distinct. In this phase, the parenchyma of the diverse 

splenic corpuscles are enveloped in their own capsules. At a subsequent stage, they join together to form one single 

organ and its coverings, and fuse to constitute the splenic capsule and the trabeculae, which incompletely separate 

the parenchyma. 

In this stage, it is understood that the spleen is an organ of multiple origin and that it partially preserves the 

individuality of the diverse segments of which it is comprised through the vessels that ramify in a distributive 

manner. This origin of the spleen explanes its segmental structure. Future splenic corpuscles that do not join to the 

others will form supranumerarian spleens, found in approximately 10% of all individuals, which can be located in 

any part of the abdomen and even outside of it, but are mostly located near the splenic pedicle. Polysplenia is a 

complex congenital syndrome associating visceral heterotaxis and concomitant bilateral left-sidedness. The spleen is 

divided into several splenules of the same size (Fig. 1). 


31-3274-7744; E-mail : petroian@gmail.com


With the development of the peritoneum and other abdominal organs, the spleen acquires another covering which is 

serous and is mainly joined to the stomach by the dorsal mesogastrium, which will become the splenogastric 

ligament. The splenogastric vessels are located within this ligament. The most likely origin of these vessels is 

through vaculogenesis, combining the vasculature of the gastric wall with the vessels that run throughout the 

parenchyma of the superior splenic pole. 

The main ligament that holds the spleen in place is the splenophrenic ligament, which links to the diaphragmatic 

surface of the peritoneum, and continues with the splenorenal ligament that continues with the Gerota capsule of the 

kidney and contains the final portion of the splenic hilar vessels. The lower perisplenic ligament is the phrenocolic, 

which partially involves the spleen and is responsible for connecting the left angle of the colon to the diaphragm. It 

is incorrect to call this ligament “splenocolic”, because this ligament does not connect the colon to the spleen, but 

the spleen is located inside this structure. 

Figure 1: A supranumerary spleen on the greater omentum. 

MORPHOLOGICAL ASPECTS [3,4] 

This chapter presents, in an objective manner, the morphology of the spleen, highlighting its role in different 

procedures that become necessary for surgical treatments involving the spleen. 

Macroscopic Morphology [11-15] 

To operate in a proper manner, one must understand the morphological particularities of each specific organ. In this 

light, some key morphological aspects regarding surgery of the spleen will be presented. 

Splenic ligaments [9,10,16,17] 

The spleen is an oval organ, located obliquely in the left hypochondrium and protected by the 9th and 11th ribs. It is 

held in place by the left phrenocolic, splenogastric, splenophrenic, and splenorenal (part of the phrenorenal) 

ligaments. This last ligament is directly related to the splenic pedicle vessels and to the tail of the pancreas. 

Due to congenital mal-formation or when at a more advanced age, ligaments may be looser, in turn causing splenic 

ptosis, with a stretching of the vascular pedicle. In this situation, the spleen becomes mobile or floating and can be 

palpated below the costal margin, without being increased in size, or can be found in any part of the abdomen. An 

ultra-sound exam is enough to discard a splenomegaly and clarify this situation. Possible complications of this ptosis 

include the compression or displacement of other organs, internal hernias, and twists of the splenic vascular pedicle. 

Spleen Morphology [18-22] 

The external surface of the spleen is divided into one lateral convex surface (diaphragmatic), one posteromedial 

(renal, in contact with the anterosuperior surface of the left kidney) and another anteromedial (in contact with gastric

Surgical Anatomy of the Spleen The Spleen 119 

fundus). It presents three borders: an anterior (gastric), where one or more organs can be seen; a posterior (renal); 

and a third medial (colonic, above the splenic angle of the colon). Its extremities are: the cranial (hepatic, behind the 

extremity of the left lobe of the liver) and the tail (colonic). 

Normal splenic dimensions are similar to a tightened fist, measuring 12 cm long by 8 cm wide by 3 cm thick. Its 

weight without blood is from 75 to 90 grams, with blood being between 150 and 250 grams. The spleen of a male is 

heavier than that of a woman, and its dimension is similar to a closed hand. This organ reaches its largest dimension 

in puberty and shrinks with age, especially after 60 years of age. Reports have shown spleens of only 15 grams of 

full weight in very elderly people. 

Conversely, in pathological situations, the spleen may actually retain blood and grow, taking on gigantic proportions 

with weights of more than 10 kg. Splenomegaly compresses and displaces other organs and can provoke abdominal 

discomfort, dyspepsia, respiratory restrictions and difficulty on walking. 

Vascular Morphology (Fig. 2) 

The greatest vascular variety of the organism is that of the spleen. The embryonic development of its vessels occurs 

concurrently with the hepatobiliopancreatic development and is influenced by the rotations of the primitive digestive 

tube. According to anatomy specialists, the vascular structure is particular to each people. Therefore, it is imperative 

to have an in-depth understanding of the anatomy of these vessels so as to proceed in an appropriate manner in 

surgeries which require manipulation of the spleen. 

Figure 2: Schematic design of the vascular blood anatomy of the spleen (1). Observe the stomach (2), the pancreas (3), the aorta 

(4), the portal vein (5), the celiac trunk (6), the splenic artery (7), the common hepatic artery (8), the left gastric artery (9), the 

superior mesenteric vein (10), the splenic vein (11), the inferior mesenteric vein (12), the left gastric vein (13), the dorsal 

pancreatic artery (14), the magna pancreatic artery (15), a lobular branch of the splenic artery (16), a segmental branch - superior 

pole artery - (17), a segmental affluent of the splenic vein (18), left gastro-omental artery and vein (19), a short gastric artery 

(20), a subsegmental branch (21), a trabecular artery (22) and the splenogastric veins (23). 

Arterial Architecture [6,7,9,23-29,31-49] 

The spleen is irrigated by the splenic artery, described for the first time by Julius Caesar Arantius (1571), as a 

tortuous vessel that flows toward the spleen. Even today, there is no explanation as to the tortuousness of this vessel, 

which becomes even more accentuated with age. In 82% to 86% of the cases, this artery is originated as an 

independent branch of the celiac trunk; however, it may also originate together with the hepatic artery or with the 

left gastric artery in a single trunk. Another variation is its direct outlet from the aorta.

134 The Spleen, 2011, 134-152 

The Spleen in Patients with Portal Hypertension 

Ahmed Helmy* 



CHAPTER 7 

Department of Tropical Medicine and Gastroenterology, Faculty of Medicine - Assiut University Hospitals, Egypt 

Abstract: The portal system includes all veins that carry blood from the abdominal part of the gut, pancreas, gall 

bladder, and spleen. Portal vein (5-8 cm long) is formed in front of the head of pancreas by the union of superior 

mesentric and splenic veins, and enters the liver at the porta hepatis in two main branches that have segmental 

intrahepatic distribution accompanying the hepatic artery and biliary ducts. Portal pressure, like any pressure, is 

determined by flow rate and resistance. The normal portal pressure and flow are 5 to 7 mm Hg (7-10 cm H 2O) and 

1000 to 1200 ml/min respectively. Both the increased resistance to portal blood flow (backward component) and the 

increased splanchnic blood flow (forward component) play major causative roles in the development of portal 

hypertension (PHT). Portal blood flow can be obstructed before (prehepatic), inside (intrahepatic), or after 

(posthepatic) the liver. Clinically most important are esophageal varices which are the major causes of morbidity and 

mortality due bleeding. Many of the mechanisms leading to an enlarged spleen may overlap or coexist in the same 

condition and in the same patient (infection with congestion with hyperfunction). Splenomegaly is the most 

important sign of PHT. Thrombosis of the splenic vein increases the venous pressure distal to the obstruction, which 

leads to left-sided PHT and development of collateral vessels to shunt blood around the occluded splenic vein. 

Collateral circulation may develop along three pathways. A finding of isolated gastric varices on upper 

gastrointestinal endoscopy should lead to an evaluation for PHT. Most often is the treatment of the primary disease. 

INTRODUCTION 

The Spleen 

The spleen is an organ which has an active role in immunosurveillance and hematopoiesis. It lies within the left 

upper quadrant of the peritoneal cavity in close relation with ribs 9 to 12, the stomach, the left kidney, the splenic 

flexure of the colon, and the tail of the pancreas and is normally not palpable (Fig. 1). A normal spleen is about 11 

cm in its craniocaudal length and weighs 150 grams. It is generally accepted that spleens weighing over 400 grams 

indicate splenomegaly, and some authors consider spleens weighing over 1000 grams to indicate massive 

splenomegaly. A study by Poulin et al (1998) defined splenomegaly as moderate if the largest dimension is 11 to 20 

cm and severe if the largest dimension is over 20 cm [1]. 

Figure 1: The normal size and position of the spleen. 

*Address correspondence to Ahmed Helmy: Department of Tropical Medicine and Gastroenterology, Faculty of Medicine - Assiut University 

Hospitals, Egypt; E-mail: ahsalem10@yahoo.com

The Spleen in Patients with Portal Hypertension The Spleen 135 

The four most important normal functions of the spleen [2] are: 

Synthesis of immunoglobulin G (IgG), properdin (an essential component of the alternate pathway of 

complement activation), and tuftsin (an immunostimulatory tetrapeptide). 

Clearance of microorganisms and certain antigens from the blood. 

Embryonic hematopoiesis in certain diseases. 

Removal of abnormal and aged red blood cells (RBC). 

Portal Circulation 

The portal system includes all veins that carry blood from the abdominal part of the gut, pancreas, gall bladder, and 

spleen. Portal vein (5-8 cm long) is formed in front of the head of pancreas by the union of superior mesentric and 

splenic veins, and enters the liver at the porta hepatis in two main branches that have segmental intrahepatic 

distribution accompanying the hepatic artery and biliary ducts (Fig. 2). 

Figure 2: Anatomy of the portal venous system. SMV; superior mesenteric vein. SV, splenic vein. IMV; inferior mesenteric 

vein. PV; portal vein. LGV; left gastric vein. HVs; hepatic veins. IVC; inferior vena cava. 

Portal Hypertension 

Portal pressure, like any pressure, is determined by flow rate and resistance. The normal portal pressure and flow are 

5 to 7 mm Hg (7-10 cm H2O) and 1000 to 1200 ml/min respectively. Portal O2 content represents approximately 

72% of the total oxygen supply to the liver. Both the increased resistance to portal blood flow (Backward 

Component) and the increased splanchnic blood flow (Forward Component) play major causative roles in the 

development of portal hypertension (PHT), which is defined as an increase in portal venous pressure >10 mmHg. 

Portal blood flow can be obstructed before (prehepatic), inside (intrahepatic), or after (posthepatic) the liver (Table 

1). However, a combination of these can exist; for example, extrahepatic portal vein thrombosis may be 

accompanied by obliteration of intrahepatic portal vein branches. Increased blood pressure in the portal system leads 

to the development of splenomegaly and collateral circulation associated with ectatic veins or varices at different 

sites in the abdomen and pelvis (Table 2, Fig. 3). Clinically most important are esophageal varices which are major 

causes of morbidity and mortality due bleeding. Ectatic veins in the gastric and colonic mucosa are the morphologic 

substrates of portal gastropathy and colopathy. PHT is responsible for most of the complications of cirrhosis 

including splenomegaly and hypersplenism [2].

136 The Spleen Ahmed Helmy 

Table 1: Causes and classification of PHT. 

Pre-hepatic PHT: 

Primary* 

Splenic vein thrombosis, invasion or compression. 

PV anomalies, thrombosis, invasion or compression. 

Umbilical vein sepsis or congenital anomalies. 

Hepatic PHT: (pre-sinusoidal, sinusoidal and post-sinusoidal) 

Pre-sinusoidal: 

Schistosomal hepatic fibrosis 

Congenital hepatic fibrosis 

Infiltrations with sarcoidosis, myeloproliferative disorders, Hodgkin's disease, leukemia 

Idiopathic 

Sinusoidal: 

Liver cirrhosis (commonest). 

SOS: recent evidence of sinusoidal involvement. 

Post-sinusoidal: This can be hepatic or suprahepatic. 

Hepatic: as in SOS involving the small hepatic venules. 

Suprahepatic: Obstruction can be at the level of: 

Hepatic veins/IVC: thrombosis, web, tumor, Budd-Chiari syndrome. 

Heart: high right atrial pressure as in constrictive pericarditis. 

PHT; portal hypertension. SOS; sinusoidal obstruction syndrome. IVC; inferior vena cava. *; Primary PHT occurs due to increased blood flow through 

an enlarged spleen as in idiopathic tropical splenomegaly, Cruvellhier Baumgarten syndrome, blood dyscrasias, and hepatoportal arteriovenous fistulae. 

Figure 3: Sites of portal-systemic collaterals that open in patients with portal hypertension (PHT).

The Spleen, 2011, 153-178 153 

Benign Vascular, Cystic and Solid Diseases of the Spleen 

Eelco de Bree, Vasilis Charalampakis and John Melissas* 

Department of Surgical Oncology, University Hospital, Heraklion, Greece 



CHAPTER 8 

Abstract: As benign, non-traumatic, splenic diseases are extremely rare, the practicing surgeon very occasionally 

deals with patients suffering from such conditions. A number of these diseases, such as congenital splenic cyst, may 

present themselves with mild symptomatology, thereby creating diagnostic uncertainty. Others however, such as 

hydatid cyst, when unprofessionally managed, may still be dangerous and even prove lethal. Therefore, the diagnosis 

and management of benign non-traumatic splenic diseases remain a challenge for the clinician. Benign splenic 

diseases, which are discussed in this chapter, include non-parasitic cysts (primary or true and secondary or false 

cysts), inflammatory cystic masses (hydatid cyst, bacterial and fungal abscesses), benign vascular neoplasms 

(haemangioma, littoral cell angioma, lymphangioma and hamartoma), benign vascular pathology (splenic infarction, 

splenic artery and vein aneurysm, intrasplenic pseudoaneurysm, splenic arteriovenous fistula and splenic vein 

thrombosis), and other benign disorders such as inflammatory pseudotumour of the spleen, splenic peliosis, Gandy- 

Gamna’s bodies and ectopic or wandering spleen. Their signs and symptoms are vague, non-specific and often 

confusing, delaying and often making diagnosis difficult. Clinical findings and blood analysis are often of little help. 

Sonography, computed tomography and magnetic resonance imaging are the most valuable imaging techniques. 

Besides being a therapeutic procedure, surgery may be indicated when the diagnosis is in doubt. While splenectomy 

was the treatment of choice for a long period of time, during the last decades, more conservative management has 

been advocated for benign non-traumatic splenic disorders after the recognition of the significant function of the 

spleen. Additionally, improvement in available equipment and an increasing experience of interventional radiologists 

under emergent conditions has led to increased application of endovascular techniques in the treatment of diseases of 

the splenic vessels and subsequent preservation of splenic function. 

INTRODUCTION 

As benign, non-traumatic, splenic diseases are extremely rare, the practicing surgeon very occasionally deals with 

patients suffering from such conditions [1,2]. A number of these diseases, such as congenital splenic cyst, may 

present themselves with mild symptomatology, thereby creating diagnostic uncertainty. Others however, such as 

hydatid cyst, when unprofessionally managed, may still be dangerous and even prove lethal. Therefore, the 

diagnosis and management of benign non-traumatic splenic diseases remain a challenge for the clinician [1,2]. 

Benign splenic diseases, which are discussed in this chapter, include non-parasitic cysts (primary or true and secondary 

or false cysts), inflammatory cystic masses (hydatid cyst, bacterial and fungal abscesses), benign vascular neoplasms 

(haemangioma, littoral cell angioma, lymphangioma and hamartoma), benign vascular pathology (splenic infarction, 

splenic artery and vein aneurysm, intrasplenic pseudoaneurysm, splenic arteriovenous fistula and splenic vein 

thrombosis), and other benign disorders such as inflammatory pseudotumour of the spleen, splenic peliosis, Gandy- 

Gamna’s bodies and ectopic or wandering spleen (Table 1). Their signs and symptoms are vague, non-specific and often 

confusing, delaying and often making diagnosis difficult. Clinical findings and blood analysis are often of little help, so 

that imaging studies and surgical intervention are usually needed to establish a correct diagnosis [1-3]. Sonography, 

computed tomography and magnetic resonance imaging are the most valuable imaging techniques [3-12]. 

BENIGN CYSTIC DISEASE 

Nonparasitic Splenic Cysts 

Splenic cysts are rare and problems with their classification are frequent, although for almost a century this 

classification has occupied our profession [13]. Fowler [14], in 1913, classified them as parasitic and nonparasitic 

based on aetiology. Actually, parasitic cysts of the spleen are almost exclusively hydatid cysts, which have been 

*Addres correspondence to John Melissas: Department of Surgical Oncology, University Hospital, P.O. Box 1352, 71110 Heraklio; Tel: +30- 

2810-392387; Fax: +30-2810-542090; E-mail: melissas@med.uoc.gr

154 The Spleen Bree et al. 

Table 1: Benign vascular, cystic and solid diseases of the spleen discussed in this chapter. 

Benign cystic disease of the spleen 

Non-parasitic splenic cysts Hydatid cyst 

Splenic abscess 

Benign vascular neoplasms of the spleen 

Haemangioma 

Littoral cell angioma 

Lymphangioma 

Hamartoma 

Benign vascular pathology of the spleen 

Splenic infarction 

Splenic artery aneurysm 

Intrasplenic pseudoaneurysm 

Splenic vein aneurysm 

Splenic arteriovenous fistula 

Splenic vein thrombosis 

Other benign disorders of the spleen 

Inflammatory pseudotumour Splenic peliosis 

Gamna-Gandy’s bodies 

Wandering spleen 

discussed previously and are totally different from non-parasitic cysts. Fowler classified nonparasitic cysts of the 

spleen as true cysts (considered to be primary cysts) and false or pseudocysts (considered to be secondary cysts) 

based on the presence or absence of lining epithelium [14]. True cysts can be only partially lined by epithelial cells, 

possibly because of pressure degeneration, and multiple sections from different parts of the cystic wall are required 

to reveal the cellular lining. Misdiagnosis may occur when the epithelium is not continuous and existent portions of 

epithelium fail to be disclosed [15]. Subsequently, many different, complicated and controversial classifications 

have been suggested [13]. Polyphony in classification reflects the poor understanding of the histopathogenesis of 

nonparasitic splenic cysts. True cysts are generally divided in congenital and neoplastic cysts. Multiple terms for 

primary splenic cysts of congenital origin have been used. Recently, Morgenstern defined the congenital cysts and 

included the histological types of epithelial, epidermoid, mesothelial, serous, and transitional cysts in this category 

[15]. In addition, there has been no clear distinction between congenital and neoplastic cysts. In various 

classifications, epidermoid and dermoid cysts have been included among either neoplastic or congenital cysts [13]. 

Most recently, a new classification has been proposed (Table 2), in which nonparasitic splenic cysts are divided in 

primary and secondary cysts [13]. This distinction is based on their different aetiology. 

A primary cystic cavity can result from compaction of mesothelial cells included during development (congenital 

cysts), aberrant germ cells (dermoid cysts) or vessel formation (angiomas) [13]. The superficial location of 

congenital cysts in the spleen supports the suggestion that these cysts originate from capsular mesothelial cells 

migrating into the spleen [16]. In congenital cysts, metaplasia of the mesothelium lining into transitional or stratified 

squamous epithelium may occur [13,15]. The corresponding translational and so-called ‘epidermoid cysts’ are 

included in the same category of congenital cysts [13]. Dermoid cysts and angiomas are considered neoplastic cysts. 

The most common type of neoplastic splenic cysts is angioma of either blood vessels (haemangioma) or lymph 

vessels (lymphangioma). Splenic haemangioma can be capillary or cavernous [13,16]. Some authors suggest that 

splenic angiomas should not be considered cysts, but rather cystic tumours [17,18]. However, others consider cystic 

tumours (e.g. cystadenomas) to be derived from epithelial cells, usually glandular, forming cystic masses, while the 

lining of the wall of angioma consists of endothelium [13]. Angiomas will be discussed later under a separate 

heading in more detail. Dermoid cysts of the spleen are rare and contain elements of ectodermal origin, such as hair, 

sebaceous material, and keratin [13]. Aberrant germ cells in the spleen can reach a critical mass and undergo

Benign Vascular, Cystic and Solid Diseases of the Spleen The Spleen 155 

compaction, which would create the cystic cavity. At the same time, germ cells of the cystic wall, which are 

multipotential, can differentiate toward ectodermal tissues. Because these cysts consist of many well-differentiated 

tissues but in ectopic location they are, by definition, benign teratomas and share the same histology with dermoid 

cysts of the ovary [13]. 

Table 2: Classification of nonparasitic splenic cysts according to Mirilas et al. [13]. 

Classification Criteria 

Primary nonparasitic splenic cysts 

Congenital 

Neoplastic 

Angiomas 

Haemangiomas 

Lymphangiomas 

Dermoid cysts 

Secondary nonparasitic splenic cysts 

Traumatic 

Necrotic 

Cystic lining: mesothelial, transitional and/or stratified squamous 

Gross appearance of cyst (interior): glistening white colour, 

trabeculation 

Cystic lining: endothelial 

Blood content in cyst 

Lymph content in cyst 

Cystic lining: ectopic, mature ectodermal tissues 

Positive trauma history 

Gross appearance of cyst (interior): “shaggy, haemorrhagic, 

normal splenic architecture 

Cystic wall: thick, collagenous 

Infarct: pain left upper quadrant 

History of active bacterial infective endocarditis 

Nonspecific acute splenitis: e.g. typhoid fever, infectious 

mononucleosis, blood dissemination of haemolytic streptococcus, 

generalized lymphadenopathy 

Secondary cysts account for 70% to 80% of nonparasitic cysts of the spleen [19]. They are more frequent in teenagers 

and young adult men [20]. Although nonparasitic splenic cysts remain rare, the incidence appears to be rising, possibly 

due to the frequent use of abdominal imaging and the increasingly successful nonoperative management of splenic 

injuries [21,22]. In secondary splenic cysts, a primary event (trauma, infarct, or inflammation) leads to secondary 

formation of the cystic cavity, which is subsequently organized circumferentially and obtains a cystic wall deprived of 

cellular lining [13,15]. Secondary cysts are divided in traumatic and necrotic cysts. Trauma is the most common cause 

and leads to subcapsular or intrasplenic haematoma, i.e. haemorrhagic cystic cavity [13,15]. The cystic wall is developed 

of fibrous tissue. Traumatic cysts have a thick collagenous wall with spotty calcification, and a shaggy haemorrhagic 

interior with clear evidence of normal splenic architecture, they may contain brown or brownish-green fluid, probably 

from the breakdown of blood [15,20]. Less frequently, secondary cysts are caused by splenic infarction and 

inflammation, leading to liquefaction necrosis because of hydrolytic enzyme activation. The necrotic area, containing 

tissue debris and fluid, constitute the cystic cavity. In necrotic cysts, their boundaries become organized circumferentially 

with fibrous tissue and create a wall around the necrotic cavity [13]. 

Most nonparasitic splenic cysts are probably asymptomatic. Symptoms and signs are non-specific, including abdominal 

pain, left shoulder pain, palpable mass and early satiety [21,23]. Since they are susceptible to haemorrhage, rupture and 

infection, nonparasitic cysts larger than 5 cm in diameter should be managed surgically, even when asymptomatic [24]. 

At sonography, a well defined anechoic mass is seen. In the case of secondary cysts, internal echoes from debris and 

peripheral brightly echogenic foci with distal shadowing due to calcifications within the fibrous wall may be seen 

[11]. Computed tomography shows a low-attenuation, unilocular mass with imperceptible walls; the attenuation of

The Spleen, 2011, 179-191 179 



CHAPTER 9 

Chronic Lymphocytic Leukemia, Follicular Lymphoma and the Spleen 

André Márcio Murad and Andy Petroianu* 

Department of Clinics and Department of Surgery, Medical School - Federal University of Minas Gerais 

Abstract: Chronic lymphocytic leukemia (CLL) is a clonal malignancy that results from expansion of the mature 

lymphocyte compartment and is the most common leukemia in adults. The survival period from the time of 

diagnosis of CLL varies between 2 and more than 10 years. At the time of diagnosis, most patients with chronic 

lymphocytic leukemia does not need to be treated with chemotherapy until the patient is symptomatic. 

Chlorambucil and cyclophosphamide were the main therapy in CLL. Cyclophosphamide is usually combined 

with other agents, such as vincristine and prednisone, and incorporated into combination regimens. High response 

rates were also seen with anthracycline regimens. Purine analogues are currently used in CLL. Because of the 

difficulty in eradicating CLL cells from bone marrow peripheral blood, autologous transplantation is widely used. 

Rituximab, an anti-CD20 monoclonal antibody, has recently provoked interest for the treatment of CLL. Perhaps 

the most potent regimen for CLL is the combination of the most effective single chemotherapeutic agent with the 

most effective monoclonal antibody. Splenectomy is helpful in the management of selected patients with CLL, 

who do not present adequate response to clinical therapy in an attempt to reduce the resistance to drugs and to 

alleviate the symptoms provoked by the huge size of the spleen. Besides the advantages of splenectomy, it must 

be stressed that in most cases this procedure is accompanied by a greater morbidity and mortality. Thus a 

conservative procedure that reduces the spleen size may have a similar effect to that of total spleen ablation for 

treatment of CLL, without losing the important functions of this organ. Subtotal splnectomy or splenic 

autotransplants after total splenectomy are worth to be considered as surgical options in presence of a 

symptomatic giant spleen or a refractory patient to chemotherapy. 

Key Words: Spleen, Leukemia, Lymphoma, Chemotherapy, Surgery, 

INTRODUCTION 

Chronic lymphocytic leukemia (CLL) is a clonal malignancy that results from expansion of the mature lymphocyte 

compartment. This expansion is a consequence of prolonged cell survival, despite a low proliferating index. The 

affected lymphocytes are of B-cell lineage in 95% of cases, and the remaining cases involve T lymphocytes. CLL is 

the most common leukemia in adults in western countries, and it accounts for approximately 25% of all leukemias. 

The proportion of cases diagnosed in the early stages of the disease has risen from 10% to 50%, probably because of 

improved diagnosis [1]. 

The survival period from the time of diagnosis of CLL varies between 2 and more than 10 years, depending on the 

stage. The staging systems of Rai et al [2] and Binet et al [3] are used to estimate prognosis. Both are based on the 

extent of lymphadenopathy, splenomegaly, and hepatomegaly. Physical exam, the degree of anemia and 

thrombocytopenia in peripheral cell counts are other important parameters of prognosis in CLL. These simple 

studies are inexpensive and can be applied to every patient without technical equipment. Both staging systems 

describe three major prognostic subgroups (Table 1). 

Splenectomy is helpful in the management of selected patients with CLL, who do not present adequate response to 

clinical therapy in an attempt to reduce the resistance to drugs and to alleviate the symptoms provoked by the huge 

size of the spleen. Besides the advantages of splenectomy, it must be stressed that in most cases this procedure is 

accompanied by a greater morbidity and mortality, mainly due to sepsis. 

*Address correspondence to Andy Petroianu: Avenida Afonso Pena, 1626 - apto. 1901, Belo Horizonte, MG 30130-005, Brazil; Tel / Fax : 55 

- 31 - 8884-9192; E-mail : petroian@gmail.com

180 The Spleen Murad and Petroianu 

The severity of the adverse effects of total splenectomy are responsible for the exclusion of this surgical treatment in 

patients with leukemia. In fact, the purpose of the splenectomy is not to make the patient asplenic, but only to obtain 

a better therapeutical response. Thus a conservative procedure that reduces the spleen size may have a similar effect 

to that of total spleen ablation for treatment of CLL, without losing the important functions of this organ. Subtotal 

splnectomy or splenic autotransplants after total splenectomy are worth to be considered as surgical options in 

presence of a symptomatic giant spleen or a refractory patient to chemotherapy. 

Table 1: Staging systems for chronic lymphocytic leukemia [2-3]. 

Stage Lymphocytosis Lymphadenopathy 

Hepatomegaly or 

splenomegaly 

Other features 

Median 

survival 

(years) 

0 + x 

Rai staging system 

x - >10 a 

I + + x - 7 b 

II + +/x + - 7 b 

III + +/x +/x Anaemia 1.5-4 c 

IV + +/x +/x Thrombocytopenia 1.5-4 c 

Binet staging system 

A + +/x d +/x - 12 

B + +/x e +/x - 7 

C + +/x +/x Anaemia and 

thrombocytopenia 

2-4 

a Survival for low-risk patients (stage 0) 

b Survival for intermediate-risk patients (stages I and II). 

c Survival for high-risk patients (stages III and IV). 

d < 3 areas of clinical lymphadenopathy. 

e >3 areas of clinical lymphadenopathy. 

Symbols: + = present; x = absent; +/x = may be present or absent;- = no other distinguishing features. 

NEW RESEARCHES IN CHEMOTHERAPY OF CLL 

As with other malignancies, eradication of the disease is a desired endpoint of CLL treatment, especially in younger 

patients. New detection technologies have found that most patients who achieve a complete response as defined by 

the National Cancer Institute-sponsored working group (NCI-WG) guidelines typically have minimal residual 

disease (MRD) [4]. Critical in this assessment is a standardization of the techniques used to define MRD. The most 

sensitive techniques are four-colour flow cytometry and real-time quantitative polymerase chain reaction (PCR). 

Conservative management is the main purpose of the treatment in leukosis. However in selected patients with CLL 

splenectomy is imposed by the discomfort of the huge spleen that also leads to an ineffective chemotherapy. 

Although splenectomy is helpful in the management of patients with CLL, in most cases this procedure is 

accompanied by a greater morbidity and mortality, mainly due to sepsis. These adverse effects are responsible for 

the exclusion of surgical treatment in most patients with leukemia. Total splenectomy indicated for patients who do 

not present adequate response to clinical therapy in an attempt to reduce the resistance of the patient to drugs and 

alleviate the symptoms due to the huge size of the spleen. In fact, the purpose of the splenectomy is not to make the 

patient asplenic, but only to obtain better clinical results. Thus it may be proposed that a conservative procedure that 

reduces spleen size may have an effect similar to that of total spleen ablation for treatment of CLL. 

Response Assessment Including Minimal Residual Disease 

Any decision to treat CLL should be guided by clinical staging, the presence of symptoms, and the disease activity. 

Evidence that current treatment can improve outcome is only available for patients with Rai III and IV or Binet B

Chronic Lymphocytic Leukemia, Follicular Lymphoma The Spleen 181 

and C stages. Patients in earlier stages (Rai 0-II, Binet A) are generally not treated but monitored with a "watch and 

wait" strategy. 

At the time of diagnosis, most patients with chronic lymphocytic leukemia (chronic lymphoid leukemia, CLL) does 

not need to be treated with chemotherapy until the patient is symptomatic, or there is evidence of rapid progression 

of disease characterized by: 

Weight loss of more than 10% over 6 months 

Extreme fatigue 

Fever related to leukemia for longer than 2 weeks 

Night sweats for longer than one month 

Progressive marrow failure (anaemia or thrombocytopenia) 

Autoimmune anaemia or thrombocytopenia not responding to glucocorticoids 

Progressive or symptomatic splenomegaly 

Massive or symptomatic lymphadenopathy 

Progressive lymphocytosis, as defined by an increase of greater than 50% in 2 months or a doubling 

time of less than six months. 

In early stages, treatment is necessary only if symptoms associated with the disease occur (e.g., B symptoms, 

decreased performance status, or symptoms or complications from hepatomegaly, splenomegaly, and 

lymphadenopathy). High disease activity, often defined by a lymphocyte doubling time of less than 6 months or by 

rapidly growing lymph nodes, is also an indication to treat. In contrast, even in advanced disease (Rai III and IV or 

Binet C), the absence of disease progression (e.g., with a stable platelet count around 80,000/µl) may sometimes 

justify a "watch and wait" strategy. 

Alkylating Agents 

During four decades, chlorambucil and cyclophosphamide were the main therapy in CLL [5]. Both drugs are well 

absorbed orally and have a favourable toxicity profile. A variety of different schedules of chlorambucil are used, but 

none have been defined to be superior to any other, and the major toxicity with chlorambucil remains 

myelosuppression. 

Cyclophosphamide is usually combined with other agents, such as vincristine and prednisone, and incorporated into 

combination regimens such as CVP or COP. The addition of prednisone stems from evidence that corticosteroids are 

useful in the management of autoimmune hemolytic anaemia and thrombocytopenia. However, as single agents, 

they have only modest activity and their extended use in CLL exposes patients to the risk of infection. In a variety of 

therapeutic trials, no clear evidence has emerged that any one alkylating agent regimen is superior to another [5,6]. 

Anthracycline Combinations 

Neither anthracyclines nor vinca alkaloids have demonstrated single-agent activity in CLL, presumably because of 

the high frequency of elevated mdr1 expression in CLL cells. Nevertheless, a variety of combination regimens have 

been evaluated based on the CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) regimen used in 

lymphoma. Although the CR rates appear to be higher with CHOP than with chlorambucil plus prednisone, no 

survival advantage has been noted [7]. Of note, a high-dose chlorambucil regimen showed a superior response rate 

and equivalent survival to the CHOP regimen. 

High response rates with no significant survival advantage were also seen with two other anthracycline regimens: 

CAP (cyclophosphamide, doxorubicin, and prednisone) and POACH, which employs the same three-drug 

combination plus the addition of ara-C and vincristine [8].

192 The Spleen, 2011, 192-200 

Primary and Metastatic Cancer of the Spleen 

Jörg Sauer* 

Karolinen-Hospital Hüsten, Department of General and Visceral Surgery, D-59759 Arnsberg 



CHAPTER 10 

Abstract: Malignant diseases of the spleen occur rather frequently. However, most of these cases are malignant 

diseases of the lymphatic and haematopoietic systems, but not local malignant neoplasms of the spleen. Most 

frequently, such diseases come with an enlargement of both the entire spleen and the lymph nodes of the splenic 

hilum. A systematic treatment of the underlying disease should be given priority over a splenectomy, which may be 

applied in particular cases only. It should be noted, that in order to diagnose properly or stage the systemic disease a 

splenectomy including the removal of the splenic hilum may become inevitable. Notwithstanding, in most of today’s 

cases, imagining diagnostics is an appropriate means to identify an affection of the spleen. Malignant neoplasms in 

the spleen are very rare. Most tumours can be identified and categorised through the use of anamnesis, imaging, 

chemical and laboratory examinations. If malignant neoplasms have isolatedly affected the spleen, splenectomy can 

be applied to cure the organ. Generally, the splenectomy can be conducted in a laparoscopic way. The use of 

splenectomy is not reasonable in patients with more organs affected; such cases require a systemic therapy. 

INTRODUCTION 

Malignant diseases of the spleen occur rather frequently. However, most of these cases are malignant diseases of the 

lymphatic and haematopoietic systems, but not local malignant neoplasms of the spleen. Most frequently, such 

diseases come with an enlargement of both the entire spleen and the lymph nodes of the splenic hilum. 

A systematic treatment of the underlying disease should be given priority over a splenectomy, which may be applied 

in particular cases only. It should be noted, that in order to diagnose properly or stage the systemic disease a 

splenectomy including the removal of the splenic hilum may become inevitable. Notwithstanding, in most of today’s 

cases, imagining diagnostics is an appropriate means to identify an affection of the spleen (Table 1). 

Table 1: Imaging diagnostics for detecting changes of the spleen 

Sonography 

Colour duplex sonography 

Computed tomography (CT) 

Magnetic resonance tomography (MRT) 

Positron emission tomography (PET) 

Positron emission computed tomography (PET-CT) 

Scintigraphy 

The histological build up of the spleen, which is basically composed of the endothelium and lymphatic tissue, prevents this 

organ from developing carcinoma, thus limiting primary local tumours to a certain sarcomatous form, namely 

angiosarcoma. Contrary to that, all metastasising solid tumours occurring can develop metastases in the spleen. 

PRIMARY CANCER 

Leukemia 

The most frequently occurring forms of primary malignant diseases, with the spleen involved, are lymphoma and 

leukemia. 

*Address correspondence to Jorg Sauer: Karolinen-Hospital Hüsten, Department of General and Visceral Surgery, D-59759 Arnsberg; E-mail: 

joerg_sauer@gmx.net

Primary and Metastatic Cancer of the Spleen The Spleen 193 

Modern medicine distinguishes three different forms of leukemia. The fourth form, the so-called chronic lymphatic 

leukemia, is a low-grade non Hodgkin’s lymphoma, which develops in a leukemic way, making it a lymphoma 

disease. Leukemia generally brings about a diffuse enlargement of the spleen, without making the single lesions in 

the spleen visible. There is currently no treatment of the spleen specially designed for leukemia. Of course, a 

systemic therapy that also includes a treatment of the spleen appears sufficient; any splenectomy should only applied 

when occurring complications require so. For specific issues regarding the symptoms and signs, diagnostics and 

treatment of leukemia, I would like to refer to the standard works of haematology, where you will have answered 

your questions thoroughly. (Table 2). 

Table 2: Types of leukemia 

Acute myeloid leukemia (AML) 

Acute lymphatic leukemia (ALL) 

Chronic myeloid leukemia (CML) 

Malignant Lymphoma 

In patients with malignant diseases of the lymphocytopoiesis, diffuse enlargements and infiltrations of the spleen, 

miliary (< 2 cm) and large tumours in the spleen as well as enlargements of the lymph nodes in the splenic hilum 

may occur. Necroses in larger lymphomas can bring about cystic space-occupying lesions [1]. Hodgkin’s and non 

Hodgkin’s lymphomas show no differences in their macroscopic change patterns, thus preventing us from deferring 

the entity from the affected spleen. The differentiation of the Hodgkin’s lymphoma into stages of development, 

however, is has been made on the grounds of the way the spleen is affected. The pathology of lymphomas varies; 

not all of them affect the spleen, which is considered the largest lymphatic organ. Even the symptoms and signs, 

diagnostics and treatment of leukemia is dealt with comprehensively in the standard works of haematology, so that 

this paper provides only one table (Table 3) showing the different non Hodgkin’s lymphomas and a labelling of the 

entities most frequently affecting the spleen. 

Table 3: Types of Non-Hodgkin lymphomas and frequent affection of the spleen 

B-cell lymphomas X 

Indolent / low grade NHL 

Chronic lymphatic leukemia (B-CLL) 

Prolymphocytic leukemia (B-PLL) 

Hairy cell leukemia (HCL) X 

Immunocytoma / lymphoplasmocytic lymphoma 

Multiple myeloma 

Marginal zone B-cell lymphoma of MALT type (mucosa-associated-lymphatic tissue) 

Follicular lymphoma (stages I, II, III) 

Aggressive / high grade NHL 

Diffuse large B-cell lymphoma 

Mantle cell lymphoma (MZL) X 

Mediastinal B-cell lymphoma 

Burkitt’s-lymphoma 

Burkitt’s-like lymphoma 

Precursor of B-cell lymphoblastic leukemia (acute lymphatic leukemia, ALL) / lymphomas 

Sarcoma 

An angiosarcoma can develop in a spleen. The frequency of occurrences of this tumour is rather low. In 1992 

Westhoff reports a total of 135 publicised cases [2]. This tumour may occur in all stages of life. Because of its lack

194 The Spleen Jörg Sauer 

of symptoms in the early stage of disease, the angiosarcoma of the spleen is often to be found at a late and nolonger-treatable 

stage. If symptoms occur, they will be quite naturally be unspecific, as is the case with all isolated 

tumours of the spleen. 50% of all patients already show a liver metastasis with hepatomegaly. In 30% of the 

patients, the spleen ruptures spontaneously [3, 4]. 70% of the patients suffer from anaemia [3]. Thrombocytopenia 

and coagulopathy are also frequently occurring complications of these tumours. The imaging of sonography and 

computer tomography indicates inhomogeneous tumours of every size, which is accompanied by a regionally 

varying absorption of contrast media. Even scintigraphy is not coherent; we usually see uncharacteristic defects of 

the storage ability. Pathologically speaking, these are grey-white, brown or red tumour knots of different sizes, 

revealing numerous variants when examined by a microscope [2-4]. The endothelial genesis of the malignant 

neoplasm can be detected by the factor-VIII antigen [5]. As angiosarcomas can develop in all vessels and 80% of 

them are at the time of the diagnosis already metastasised, the attributing of the primary tumour with an organ is not 

always an easy task and the largest tumour is generally declared to be the primary tumour. Therefore, no incidence 

can be assigned. The genesis of angiosarcomas in the spleen is not obvious. The agents (polyvinylchloride, arsenic, 

organophosphates, thorotrast), that have been detected in liver angiosarcomas and stimulate the development of 

malignant neoplasm, can not simply be adopted for use with the spleen, because these substances could be detected 

in the anamnesis of the patients in singular cases only [6-8]. A final diagnosis, and at the same time the first step 

towards treatment constitutes the splenectomy. Bad prognoses for the tumour require an adjuvant treatment, but due 

to the small number of cases that would not justify chemotherapy, such a treatment is currently not approved. The 

findings of the different conducted chemotherapies proved to be below expectations [10]. Even after the most 

promising treatment, the one including doxorubicin and ifosfamid, no remission or curing occurred [2]. Considering 

these poor results, the search for better medication has to be continued. The median survival time is 4 months. 80% 

of all patients die within 6 months after the detection of the tumour. The specific time of the splenectomy has a 

decisive effect on the prognosis. It has to be completed before the spontaneous rupture of the spleen. Patients having 

been splenectomised prior to the rupture, have a survival time extended by 11 months [2, 11]. A cure that is worthy 

of the name occurs in individual cases only [12]. 

Metastatic Cancer 

Metastases of carcinomas in the spleen are rather rare, but not as rare as commonly suggested. The occurrence of 

metastases of a malignant neoplasm in the spleen has by now not been adequately quantified. Most publications 

dealing with the frequency of occurrences are autopsy cases [13-16]. Because of their selective approach (of 

malignant tumours of deceased people), these case studies cannot be exploited for generating epidemiological 

findings. The greatly differing frequencies of occurrence (0% to 32% metastases of the spleen in autopsied patients 

with malignant neoplasms) of the single studies are evidence of the insufficient validity. The years during which the 

largest of these studies were being conducted are characterized by a limitation of a possible detection of 

intraabdominal processes to either large space-occupying lesions or massive symptoms, thus increasing the 

likeliness of malignant neoplasms to be metastasised in a more space-occupying way before their detection. Quite 

logically, the frequent occurrence of metastases in the spleen in autopsy studies, which concentrate on patients who 

died as a result of malignant neoplasms, truly makes sense. Likewise, metastases in the spleen of living patients 

could have been detected especially in cases of intraabdominal bleedings due to a “spontaneous rupture of the 

spleen.” This explains the low frequency of metastases in clinical studies or cross-sectional autopsy studies. As there 

have been no valid findings about the frequency of occurrence, any discussing of the assumed “resistance of the 

spleen” against metastases or a supposed “preference of metastases to affect the spleen” would therefore be 

pointless. Considering the latest figures, all attempts being made so far to explain both supposedly real phenomena 

will have to be put to the test [17]. A recent epidemiological study, which evaluates the data of a large and 

comprehensive cancer registry including more than 25,000 patients with malignant neoplasms, showed that the 

spleen has been affected by metastases in only 0.97% of all cases. The overall metastasising rate of all malignant 

neoplasms of the spleen stood at a 0.002% [17]. Any notion about the frequency of occurrence of metastases will 

remain a snapshot, valid only at a particular time, because the diagnostic and therapeutic options must be seen in 

progress, which changes the frequencies at the particular points in time. Some changes can already be seen since the 

first cross-sectional autopsy study was conducted in 1974 in patients from Malmoe [13]. The frequency of all 

malignant metastases could be reduced from 62% (Malmoe, 1974) to 21% (our data). Also, the frequency of 

metastases in the spleen has been reduced, from 7% to well below 1%. Even given the autopsy study has detected 

more cases with metastases than had been previously detected in the clinical course, this demonstrates a significant

The Spleen, 2011, 201-216 201 

Pre- and Postoperative Care for Surgical Procedures on the Spleen 

Mircea Dan Venter* 

Department of Surgery, Emergency Clinical Hospital, Bucharest, Roumania 



CHAPTER 11 

Abstract: Due to associated diseases, the function of the spleen may be modified, in turn causing certain 

complications, such as anaemia, altered coagulation, malnutrition and organ failure. Preoperative 

management of patients must take these two possibilities into account. In non-traumatic splenectomies, blood 

samples are necessary to screen for thrombophilia: antithrombin III deficiency, protein C deficiency, protein 

S deficiency and dysplasminogenemia. Complete blood count, AST, ALT, serum amylase, C-reactive 

protein, thrombin-AT-III complex and D-dimer also become necessary perioperatively. The preoperative 

management of anaemia must evaluate the risk and benefits of blood transfusion. Malnutrition increases the 

risk of postoperative complications. Antibiotics are recommended for patients who are immunosuppressed 

and in trauma. In the classical form of spleen surgery, pain is a frequent symptom, with variable intensity, 

mostly due to the pressure applied to the ribs. If the pain is not well managed by specific pills, it is better to 

make an anaesthetic block of the thoracic nerves. Thrombosis extending into the portal vein is rare; with an 

overall risk of 3.3%. Infection is the most common postoperative complication. Fever commonly appears 

between the fourth and seventh day after surgery. The risk of thromboembolic events and pulmonary arterial 

hypertension varies greatly, depending on the underlying condition for which the splenectomy is performed 

and its association with intravascular haemolysis. The most serious septic complication after splenectomy is 

the (OPSI), which brings about a prohibitory mortality rate of 50% to 90%. Prevention of postsplenectomy 

sepsis has occurred through the use of greater efforts to avoid splenectomies. 

INTRODUCTION 

Splenectomy is a procedure associated with great medical responsibility and ability; therefore, it is better to be 

performed only as a last case solution. 

PREOPERATIVE MANAGEMENT 

Due to associated diseases, the function of the spleen may be modified, in turn causing certain complications, such 

as anaemia, altered coagulation, malnutrition and organ failure. Preoperative management of patients must take 

these two possibilities into account. 

Patients from Haematology and Oncology can benefit from ultrasound investigations or abdominal CTs in an 

attempt to understand the spleen dimensions or the presence of secondary spleens. Moreover, secondary spleens may 

also be evaluated by scintigraphy with Tc-99m or In-43. 

Laboratory Exams 

In non-traumatic splenectomies, blood samples are necessary to screen for thrombophilia: antithrombin III 

deficiency, protein C deficiency, protein S deficiency and dysplasminogenemia. Complete blood count, AST, ALT, 

serum amylase, C-reactive protein, thrombin-AT-III complex and D-dimer also become necessary perioperatively. 

The statistic analysis of the laboratory exams suggest that SGOT and WBC are the most sensible and specific 

parameters to diagnose a post-traumatic abdominal injury [1]. A haematocrit of under 36% is less sensible to the 

presence of an abdominal injury but is frequently linked to severe injury. 

Some inflammation markers (Il 6, TNF, PGF, PCR) are high in polytraumatised patients, with maximum values 

commonly reached within the first hours after the trauma. 

*Address correspondence to Mircea Dan Venter: Associate Professor of the Department of Surgery of the Emergency Clinical Hospital, 

Bucharest, Romania

202 The Spleen Mircea Dan Venter 

Botha [1] analysed the variations of WBC levels within the first 24 hours after the trauma and concluded the 

following: upon admission, the WBC are high, with the predominance of lymphocites; after 3 hours, the WBC are 

13,900 ± 1,400/mmc and remain even higher than 10,000 for 2 more hours (PMN are predominant). The initial 

values of the amylase are of no importance for the immediate diagnosis. 

Poletti’s study shows that there is no specific combination upon admission, including clinical, imagistic, or 

laboratory exams which may help to exclude the presence of an abdominal injury for most abdominal contusions 

without performing a CT. A normal clinical exam, thoracic X-ray and FAST within a patient with GCS>13 will be 

unable to view 11% of the abdominal injuries, of which 33% are severe. The amount of blood lost is evaluated by 

determining the haemoglobin levels. 

Determining the haematocrit in dynamics is a routine in trauma. The initial value of haematocrit may not clearly 

reveal the amount of blood lost. Snyder’s study (Zehtabchi 2) shows that the sensibility of the initial value of the 

haematocrit in determining severe thoracic and abdominal injuries which require surgical treatment was 50%. A 

drop in haematocrit of more than 5% to 10% in 4 hours represents a sign of severe injury [2]. Likewise, 

administering intravenous liquids to these patients may lead to a drop in haematocrit caused by haemodilution, in 

turn rendering the results inconclusive. Bruns [3] reports that it is better to evaluate haemoglobin in dynamics with 

politraumatised patients. If the haemoglobin is found to be under 10 g/dl, one must search for occult bleeding. 

Nijboer [4] reports on a large number of politraumatised patients in which haemoglobin and haematocrit act in a 

similar manner; however, there is no need to determine both parameters in traumatised patients. 

Other laboratory parameters that are useful in diagnosing internal bleeding after trauma include arterial base deficit, 

blood lactate and pH. 

An arterial base deficit > 3 meq/l is correlated with major trauma. Patients with systolic blood pressures of less than 

100 mmHg should be classified as haemodynamically unstable and their blood should be a type prepared for 

possible transfusion. Baseline haematocrit, electrolytes, BUN/creatinin and a coagulation screen should be obtained. 

A urinalysis should be performed to detect blood and toxic metabolites. 

In splenic trauma, initial management should include the frequent monitoring of vital signs and haematocrit. 

Standard emergency protocols are instituted including two wide bore (16 or larger) IVs for vascular access, 

availability of 4-6 units of blood, nasogastric or orogastric tubes used to decompress the stomach (and allow for 

easier visualization and mobilization of the spleen) and Foley catheter to monitor urine output. 

In patients with a past history of multiple transfusions and those with autoimmune haemolytic anaemia, some 

difficulties in blood typing and cross-matching may occur. Platelets should not be administered preoperatively to 

patients with idiopathic thrombocytopenic purpura, as the thrombotic process may be accelerated. 

In the presence of myeloproliferative disorders with a tendency to develop thrombosis, it is useful to administer a 

low-dose of heparin twice daily and to continue this regimen for 5 days postoperatively. 

The preoperative management of anaemia must evaluate the risk and benefits of blood transfusion. Multiple 

transfusions may lead to immunosuppression and, therefore, a rise in the number of infectious complications. The 

haemoglobin is better to be kept at 10g/dl. In falciform anaemia, the preoperative value of the haemoglobin is no 

guarantee for the adequate transport of oxygen to tissues, given that this is determined by the amount of 

haemoglobin types [5]. Intra and postoperative management implies an adequate oxygen supply (to ensure that the 

existent haemoglobin is fully saturated) and stable blood parameters. 

Coagulation 

Prior literature shows no reports on the efficiency of determining coagulation screening routinely before operations 

[5]. Platelets higher than 100,000/mm 3 commonly indicate the surgical procedure to be followed. When platelets are

Pre- and Postoperative Care for Surgical Procedures on the Spleen The Spleen 203 

between 25,000 and 50,000/mm 3 , spontaneous bleeding is rare but may occur in trauma and during surgery, whereas 

platelets under 20,000/mm 3 , and especially under 10,000/mm 3 , suggest spontaneous bleeding [5]. 

In certain cases (renal failure, lymphoproliferative disorders, aspirin medication), bleeding may occur even at a 

higher platelet counts (platelet dysfunction). As a general rule, when a low platelet count is seen, it is necessary to 

stop taking aspirin for 5 to 7 days before surgery. Likewise, non-steroid anti-inflammatory drugs should be stopped 

24 to 48 hours before surgery. 

In ITP, the platelet count may be low, but its function is normal. Therefore, patients may be able to tolerate this low 

count. 

Malnutrition 

Malnutrition increases the risk of postoperative complications. 

Nutritional risk: index = (1.59 X albumin)+0.417x[(present weight / usual weight)x100] 

Results: Moderate = 83.5 to 97.5; Severe < 83.5; useful, easy to calculate, non-invasive, no dependence on patient 

collaboration and cheap. 

Arginin and glutamine stimulate the defense mechanisms, modulate the tumour cell metabolism and aid in the 

healing process. Glutamine preserves the bowel barrier and drops bacterial translocation. Intravenous or natural 

nutrition brings about a favourable postoperative evolution. 

Gallbladder Stones 

The presence of pigmentary gallbladder stones is characteristic for haemolytic and liver disorders. Spleen surgery is 

commonly associated with gallbladder surgery. 

Multiple Organ and System Failures 

Falciforme anaemia is associated with eye, bone and nervous system disorders. The purple associated with low a 

platelet count tends to lead to progressive renal failure. 

Antibiotics 

Antibiotics are recommended for patients who are immunosuppressed and in trauma. The potential risk of infection 

is explained by the low number of neutrocytes, preoperative cortisone and the immune system disorders due to 

anaesthesia and spleen removal. 

Hydroelectrolyte Management 

Haemathologic patients require a precise hydroelectrolytic management to avoid the risk of thrombosis. 

Special Considerations 

In Minkowski-Chauffard disease, the most appropriate moment to perform a splenectomy in adult patients should not 

be chosen during the deglobulisation crisis, considering that the evolution of the crisis represents a limited influence on 

a splenectomy. Rather, a splenectomy must be performed after the biliary ducts have been evaluated (ultrasound, 

cholangio-RM) so that, if gallbladder stones are present, these may be resolved during the same surgical procedure. 

Short-term hypertransfusion therapy is considered to be appropriate for patients with major preoperative 

thalassaemia; in this manner, the energy needed for vital processes and healing is preserved. Moreover, this therapy 

reduces the pressure caused by hypoxic anaemia on medular haematopoietic stem cells. Before surgery, intravenous 

nutrition is recommended to at least partially recover the weight loss. 

In hypertransfusion, it is useful to reduce excessive erythropoiesis and to prevent the occlusion of small blood 

vessels. Hypertransfusion should begin one week before surgery and should reduce the abnormal formation of red 

blood cells, while the existing abnormal red blood cells tend to disappear due to their short lifespan.

Conservative Surgical Procedures on the Spleen 

Andy Petroianu* 

The Spleen, 2011, 217-249 217 




CHAPTER 12 

Abstract: The spleen is a very important organ with many essential functions, not only in the defense of the 

organism, but also in its metabolism and immunological and the haematological systems. The most common 

manifestations of the splenic disturbances include the splenomegaly and a decrease, in the number of blood 

elements. After the removal of the spleen, 2% of adults present severe sepsis, while 5 % of children, the elderly 

people and patients with severe chronic diseases are at risk of death due to septic conditions. Most of splenic 

diseases may be treated conservatively. Operative procedures should be considered in special conditions, when all 

conservative options have been unsuccessfully depleted. Even in the presence of a severe trauma to the spleen or 

advanced haematological diseases, the best approach is a non-operative procedure. When the operation is 

unavoidable, partial (preserving the splenic vascular pedicle) or subtotal (preserving the upper splenic pole, being 

supplied only by the splenogastric vessels) splenectomies should be preferred. When a conservative procedure on 

the spleen is unfeasible, the best option is a total splenectomy combined with the transplant of autogenous splenic 

tissue on to the greater omentum. The technological advances and the progressive development of new surgical 

devices are responsible for surgical approaches with less pain, faster postoperative recovery and better aesthetical 

results without decreasing the therapeutic efficacy. The conservative splenic approach, whether clinical or 

surgical, is the best way to prevent postsplenectomy infection, by preserving the spleen immune role. The surgeon 

should choose the best surgical procedure and the size of the splenic remnant, remembering that at least 25 % of a 

normal spleen should be left. 

Key Words: Spleen, Splenectomy, Surgery, Auto-implants, Subtotal splenectomy, Partial splenectomy, Suture. 

INTRODUCTION [1-5] 

In the past, the spleen was considered a superfluous organ with no important function and could thus be removed with 

no major impact on the organism. The lack of scientific knowledge and the low interest in studies concerning the 

spleen, have led to the removal of the spleen, mostly due to diseases that presented no direct involvement with this 

organ. By contrast, when patients undergo a total splenectomy and pass through a longer follow-up period, many 

complications, including severe infections, thromboembolisms, food intake disturbances, fever, a poor control of the 

blood elements, negative influence on the liver and bone marrow functions, as well as fever, may arise (Table 1). 

The most common manifestations of the splenic disturbances include the splenomegaly and a decrease, in the 

number of blood elements. Other clinical findings, including infections, physical weakness and a delay in 

haemostasis tend to occur in more advanced conditions of the spleen. After the removal of the spleen, 2% of adults 

present severe sepsis, while 5 % of children, the elderly people and patients with severe chronic diseases are at risk 

of death due to septic conditions. This risk is sixty times higher than in people with healthy spleens. 

Most of splenic diseases may be treated conservatively. Operative procedures should be considered in special 

conditions, when all conservative options have been unsuccessfully depleted. Even in the presence of a severe 

trauma to the spleen or advanced haematological diseases, the best approach is a non-operative procedure. When the 

operation is unavoidable, partial (preserving the splenic vascular pedicle) or subtotal (preserving the upper splenic 

pole, being supplied only by the splenogastric vessels) splenectomies should be preferred. When a conservative 

procedure on the spleen is unfeasible, the best option is a total splenectomy combined with the transplant of 

autogenous splenic tissue on to the greater omentum. The protection against severe sepsis by conservative splenic 

procedures is a consensus in the literature. 


31-3274-7744; E-mail : petroian@gmail.com


Table 1: Disadvantages of the splenectomy 

Removal of the main organ responsible for the quick immunological defense 

Infection 

Increases the incidence of Sepsis 

Liver functions 

in general 

overwhelming 

Disturbances on Bone marrow functions 

Blood elements number 

functions 

Reduction of life survival 

Pyrogens fever 

When an operation is necessary, a minimally invasive approach (laparoscopy, NOTES or NOTUS), when possible, 

must be considered. The technological advances and the progressive development of new surgical devices are 

responsible for surgical approaches with less pain, faster postoperative recovery and better aesthetical results 

without decreasing the therapeutic efficacy. 

Table 2: Main splenic functions. 

GENERAL FUNCTIONS SPECIFIC FUNCTIONS 

Hematologic and Immunity Haematopoiesis 

Maturation of blood elements 

Immunoglobulin activation 

Recirculation of lymphocytes T and B 

Production Leukocytes 

Peptides 

immunoglobulin IgM 

Opsonins tuftsin 

properdin 

complement factors 

Stem cells - source of cells for organic replacement 

Storage Leukocytes 

Thrombocytes 

All metals 

Clearance Parasites 

Infection agents 

Antigenic substances 

Altered cells 

Foreign bodies 

Synthesis Precursor of hepatic functions 

Metabolism Lipids 

Cholesterol 

Bilirubins 

Amino acids 

Control Bone marrow 

Mononuclear phagocytic function 

Endocrine system 

Somatic development 

Sexual activity

Conservative Surgical Procedures on the Spleen The Spleen 219 

PATHOPHYSIOLOGY [3, 6-21] 

The spleen is a very important organ with many essential functions, not only in the defense of the organism, but also 

in its metabolism and immunological and the haematological systems. (Table 1) Due to the strong relation between 

this organ and the liver, the immunological system, including the mononuclear phagocyte system 

(reticuloendothelial system) and the haematological system in all its aspects, any disturbance in any one of these 

systems will cause a direct impact on the spleen. 

A primary disease of the spleen is very rare and most of pathological conditions of this organ directly affect the 

entire organism. Even without a perfect understanding of the spleen functions, this organ should be studied in an 

attempt to rationalise the therapeutic approach (Table 2). 

The diseases of the spleen have particular pathophysiologies and cannot be joined together, even when they seem to 

present similar manifestations, such as splenomegaly and cytopenia. Therefore, in this chapter each of the most 

common splenic disturbances will be analysed in separately (Table 3). 

Table 3: Main surgical disturbances of the spleen. 

DISTURBANCES DISEASES 

Trauma 

Congenital disturbances Larger splenic ligaments - splenic hypermobility 

Disturbance on splenic fusion - supernumerary spleen 

Hyposplenia and asplenia 

Portal system disturbances Portal hypertension 

Splenic vein and portal thrombosis 

Arterial and venous aneurisms 

Haematologic diseases Thrombocytopenic purpura 

Haemolytic anaemia thalassemia 

drepanocytosis 

spherocytosis elliptocytosis 

Hypersplenism 

Myeloid hepatosplenomegaly (myeloid metaplasia) 

Infections Abscesses 

Mononucleosis 

Aids 

Infestations Manson's schistosomiasis 

Echinococcosis 

Malaria 

Leishmaniosis 

Endocrine disturbances Somatic and sexual splenomegalic hypodevelopment 

Metabolic disturbances Gaucher's disease and other dyslipidemia 

Benign neoplasms Cysts 

Haemangiomas 

Hamartomas 

Malignant neoplasms Leukemias 

Lymphomas Hodgkin's 

non Hodgkin's 

Sarcomas 

Metastasis

250 The Spleen, 2011, 250-258 

Laparoscopic Splenectomy 

René Berindoague Neto* 



CHAPTER 13 

Santa Casa de Misericórdia de Belo Horizonte, Instituto de Ensino e Pesquisa da Santa Casa de, Belo Horizonte, 

Minas Gerais, Brazil 

Abstract: Since the first description of laparoscopic splenectomy (LS) in 1991, this technique has been adopted 

as the standard procedure for most indications for splenectomy throughout the world. The utility of LS in the 

treatment of hematologic diseases such as hereditary spherocytosis, immune thrombocytopenic purpura, and 

autoimmune hemolytic anemia is well established. LS has become the gold standard approach for normal or 

slightly enlarged spleens and is currently considered the procedure of choice. The benefits of laparoscopic 

removal of the spleen are evident to patients and surgeons alike. This approach is superior to open splenectomy in 

terms of postoperative pain, shorter postoperative hospital stay, perioperative complications, and an improved 

cosmetic result. Additionally, the period of convalescence is brief, with an early return to work or normal 

activities. The results of large series around the world are similar, with an operating time of between 60 and 90 

minutes, hospital stay of between 1 and 2 days and morbidity of less than 10% [1,2,3,4,5]. 

INDICATIONS, PATIENT SELECTION AND EVALUATION 

Splenectomy is typically an elective procedure, which allows ample time for proper preoperative work-up and 

treatment. This procedure can be applied to prevent the increased elimination of the blood’s corpuscular elements 

and to relieve symptoms caused by an enlarged spleen, possibly including abdominal distension, pain, and fullness 

or early satiety. Splenectomy can also be used for staging purposes in malignant diseases but has largely been 

replaced by other diagnostic procedures. 

In general, the indications for elective splenectomy can be divided into the following three categories (Table 1): 

treatment of symptomatic hypersplenism, 

cure and control of underlying splenic disease and 

staging of Hodgkin’s lymphoma. 

Primary hypersplenism may be caused by any of the three types of congenital red cell disorders associated with 

hemolytic anaemia: membrane disorders, hemoglobinopathies, and erythrocyte enzyme deficiencies. Secondary 

hypersplenism may be associated with myelo- and lymphoproliferative disorders, and portal hypertension. 

Idiopathic thrombocytopenic purpura (ITP) is the most common indication for surgery in 50% to 80% of patients 

treated by LS [1,2,3,6,7,8]. This approach can be considered the method of choice in symptomatic thrombocytopenia 

refractory to medical therapy, when toxic doses of steroids are required to achieve remission, or for relapse of 

thrombocytopenic purpura after an initial response to steroid therapy. Spleens in patients with ITP are normal sized 

or slightly enlarged, and consequently these patients benefit from all the advantages of minimally invasive surgery. 

However, special considerations must be taken into account in patients with splenic trauma, splenomegaly, and 

portal hypertension, as well as in those who are morbidly obese or pregnant. Haemodynamically unstable patients 

with traumatic splenic injuries are not candidates for LS. 

Morbid obesity increases the technical demands of the procedure due to reduced intra-abdominal working space and 

poorer visualization. However, morbid obesity is not a contraindication to LS, and the laparoscopic approach has 

certain advantages in these patients because its potential benefits are greater in the obese. 

*Address correspondence to Rene Berindoague Neto: Rua dos Otoni, 909 / 404, Belo Horizonte, MG, 30150-221, Brazil; Fax: (31) 32744861; 

Tel: (31) 32737489; E-mail: reneberindoague@gmail.com

Laparoscopic Splenectomy The Spleen 251 

Table 1: Indications for splenectomy 

Haematological splenic diseases 

Immune thrombocytopenic purpura (ITP) 

AIDS-associated ITP 

Thrombotic thrombocytopenic purpura 

Idiopathic autoimmune hemolytic anemia 

Hereditary spherocytosis 

Thalassemia major 

Acquired autoimmune hemolytic anaemia 

Myeloid metaplasia or myelofibrosis 

Polycythemia vera 

Chronic myelocytic leukemia 

Hairy cell leukemia 

Chronic lymphocytic leukemia 

Hodgkin’s disease 

Felty’s syndrome 

Sarcoidosis 

Gaucher’s disease 

Nonhaematologic splenic disorders 

Splenic cyst 

Splenic abscess 

Splenic tumor 

Trauma 

Splenic vein thrombosis 

Splenic artery aneurysm 

In pregnant patients, the viability of the fetus is a major consideration in determining the timing of the procedure. 

Splenomegaly also increases the technical difficulties of the procedure and is associated with a greater number of 

complications, thus requiring significant experience. Surgeons expert in LS have shown that the procedure is less 

likely to be achieved entirely laparoscopically when the spleen exceeds 25 cm in length or 1.5 kg in weight 

[3,5,9,10]. Patients with portal hypertension must be approached with caution as the risk of hemorrhage is increased. 

The underlying disease leading to splenectomy must be carefully evaluated because it may cause coagulation 

disorders and/or hematological sequels. Many patients receiving corticosteroids, chemotherapy or other 

immunosuppressive agents are at increased risk of surgically-related infections and impaired wound healing. Any 

existing preoperative conditions should be appropriately managed medically, such as through the administration of a 

stress-dose of intravenous corticosteroids immediately prior to surgery. Antibiotic prophylaxis should be applied 

immediately before surgery in the operating room. A first-generation cephalosporin is administered intravenously 

upon induction of anesthesia for surgical wound prophylaxis. Perioperative anticoagulant prophylaxis with 

subcutaneous heparin should be applied in all patients. Patients at high risk for portal and splenic vein thrombosis 

should receive anticoagulant prophylaxis for four weeks. 

Blood reserves (type-specific packed red blood cells) should be ensured before the intervention because of the possibility 

of rapid intra-operative hemorrhage. Likewise, specific hematologic deficiencies should be corrected. All anemic patients 

should receive red blood cell transfusions to increase the hemoglobin level to > 10g/dL. In severely thrombocytopenic 

patients, the availability of platelets for transfusion may be advisable. Thrombocytopenic patients require platelet 

transfusions if the absolute level drops below a threshold of 50,000 platelets/ml. These transfusions are notoriously 

ineffective prior to splenic artery ligation because the platelets are rapidly destroyed by the underlying splenic disorder. 

Several authors have advocated preoperative splenic artery embolisation to diminish the risk of intra-operative 

hemorrhage and reduce the size of the spleen, particularly in massive splenectomy [11,12]. This intervention,

252 The Spleen René Berindoague Neto 

however, is not without morbidity as up to 50% of patients require narcotic analgesics for severe post-embolisation 

pain [3,11,13]. Others complications such as pulmonary embolism or infarcts in the other organs have been reported. 

As an alternative, the same objective can be achieved intra-operatively by initial splenic artery ligation. 

The incidence of overwhelmingly postsplenectomy infection, although relatively small in the general population, is 

rather alarming in patients with immunodeficiency or hematological disorders, as is the case of most patients 

undergoing elective splenectomy. Vaccination against Streptococcus pneumonia, Haemophilus influenza and 

Neisseria meningitidis is recommended in all patients undergoing splenectomy one to two weeks before the 

procedure for optimal immunologic response. Scientific evidence indicates that splenectomy renders the patient at 

lifelong risk for increased susceptibility to infections. The most serious of these infections is overwhelming postsplenectomy 

infection, which occurs in 0.5% of trauma patients and in 10% to 20% of patients with hematologic 

diseases [3,5,12,14]. Patients aged less than 16 or with thalassemia or Hodgkin’s lymphoma appear to be a greatest 

risk for this complication. 

PREOPERATIVE IMAGING 

All adults scheduled for splenectomy should be investigated preoperatively by ultrasound to clarify spleen size and 

volume. For patients with benign hematologic diseases, ultrasonography is an appropriate technique to evaluate 

anatomic features such as spleen size, vascular conditions, and concomitant diseases (e.g., gallstones). For 

autoimmune or hemolytic disease, thin-slice spiral computed tomography (CT) may be used to detect accessory 

spleens, although its predictive value is low. In patients with malignant hematologic diseases, CT scan provides 

accurate information on splenic size and volume as well as possible lymphadenopathy at the splenic hilum and 

perisplenic inflammation or splenic infarction, which may cause severe intra-operative complications. 

Abdominal and spleen anatomy are determinant factors for adequate spleen dissection in cases of splenomegaly, and 

spleen size and volume may hinder dissection maneuvers due to the special characteristics of laparoscopic surgery. 

In recent years, advances in imaging techniques have enabled the reconstruction of virtual structures, which are 

highly useful in planning surgery and improving visualization during surgery. With preoperative 3D reconstruction 

of abdominal structures, the size and volume of the intra-abdominal viscera can be measured. 

In our recent study, the spleen and abdominal measures were assessed by 3D reconstruction of the CT scan, and we 

hypothesized that the volume and diameters of the spleen as well the shape of the abdomen, impair the surgical 

procedure [15]. We aimed to identify parameters that could preoperatively predict intra-operative or immediate 

postoperative outcome. Our results demonstrated that local anatomic and pathological features can affect and impair 

the outcome of the laparoscopic approach to splenomegaly, in terms of conversion, bleeding, operating time, and 

postoperative complications. Therefore, these anatomic factors should be taken into account when planning this kind 

of procedure in cases of splenomegaly. 

TECHNICAL ASPECTS 

Since the first LS, reported by Delaitre in 1991, several technical developments have facilitated this procedure [16]. 

Positioning of the patient, ultrasonic dissectors, articulating endovascular staplers, and bags for splenic extraction 

have contributed to a safe and reproducible procedure. 

LS may be performed using a lateral, semilateral, or anterior approach depending on surgeon preference, spleen size, 

patient characteristics, and the need for concomitant procedures. In the early years of LS, the anterior position was 

mainly applied. This position provides good access to the omental pouch and excellent visualization of the splenic 

hilum but difficulties arise in exposing and dissecting the ligamental structures, as well as the dorsal vessels and the 

splenic hilum. The anterior position is indicated when concurrent procedures need to be performed such as 

cholecystectomy and lymph node biopsies. 

It soon became apparent that LS is best carried out in the lateral position. The patient is positioned on the table with 

the left side elevated by the use of positioning devices (e.g., beanbag, foam wedges) up to a 40º-angle from the table 

surface. The lateral approach is the position of choice for many surgeons because of the better exposure and easier

Robotic Splenectomy 

Catalin Vasilescu* 

The Spleen, 2011, 259-263 259 

Fundeni Clinical Institute, Department of General Surgery, 258 Fundeni Street, Bucharest, Romania 



CHAPTER 14 

Abstract: While laparoscopic splenectomy has become the standard procedure for the surgical treatment of 

hematologic splenic disorders, the role of robotic splenectomy is still a matter of debate. The robotic equipment is 

expensive, still bulky and the surgical team needs special training. However, there are some limitations of 

laparoscopy in difficult splenectomies (massive splenomegaly, portal hypertension, partial/subtotal splenectomy 

and splenic malignancies) which can be overcome by the robotic system by means of better visualization, 

maneuverability and motion control allowing a better dissection of the splenic vessels and precise and timeefficient 

intracorporeal maneuvers. 

ROBOTIC SURGERY 

The term “robotic surgery” is not appropriate. A robotic surgical system is by definition not a “robot” as it does not 

perform surgical procedures on its own and does not involve artificial intelligence. Therefore, surgery involving the 

“robot” is best described as “computer-assisted laparoscopic surgery”. The Da Vinci system is actually a 

manipulator working on a master-slave principle. Instrument tips are electronically aligned with the instrument 

controllers. Consequently all movements of the surgeons’ hands are transmitted in real time from the instrument 

handles (master unit) to the robotic manipulator (slave unit). If one understands that the term “robot” designates a 

device autonomously capable of performing tasks based on a preset programme, then the term “surgical robot” is not 

accurate. The so called surgical robot is just a tool allowing a better visualization and intuitive movements, 

electronically filtered and scaled before transmitted to the instrument tips. Nevertheless the terms “surgical robot” 

and “robotic surgery” have become so popular both in the medical field and in mass-media that they cannot be 

changed anymore. 

Originating in the progress in spatial technology (telemanipulators for working outside space ships) and in military 

area (telesurgery), robotic surgery has a name that sounds like the most expected high technology solution. The topic 

has triggered heated discussion, although it is, after all, only a surgical tool, a new way to perform minimallyinvasive 

surgery. 

Throughout the widespread of robotic surgery, some nonmedical factors have played an important part. These main 

factors are patient pressure, pressure from the medical technology industry, particularly interested in quickly 

exploiting the large investment made in sophisticated research, even pressure from the academic medical world 

always looking for new areas that can be exploited scientifically. 

The advantages are obvious. But complaints do not lack either. Weaknesses often invoked are: longer duration of 

surgery, the lack of mobility of the surgical table during the procedure, the lack of haptic feedback, the role of the 

surgical assistance (Ligasure forceps, lavage and suction cannula) on auxiliary trocars, the need of special training 

for both operators and side assistant surgeon, the bulky equipment and costs. All the observations are real and for all 

of them there is an answer that shows that the surgical robot is not just a “fancy laparoscope”. The main problem is 

clearly the extremely high cost of equipment, especially because of the cost of consumables and maintenance that 

must be added to the initial investment. 

THE DA VINCI ROBOTIC SYSTEM 

Currently there is only one robotic surgical platform commercially available and FDA has approved the da Vinci 

*Address correspondence to Catalin Vasilescu: Fundeni Clinical Institute, Department of General Surgery, 258 Fundeni Street, Bucharest, 

Romania; E-mail: catvasilescu@gmail.com

260 The Spleen Catalin Vasilescu 

robotic system which is a robotic telemanipulator, consisting of three components: the cart with the robotic arms 

(one central arm for the camera and two or three for the instruments), the surgeon console with an integrated 

threedimensional display and the vision cart. The surgeon sits at the console, away from the patient and has a 

stereoscopic viewer, hand manipulators and foot pedals that allow him to control the camera and the robotic 

instruments inside the patient. The instruments provide both articulated motion and seven degrees of freedom 

mimicking the flexibility of human hand. The two-channel telescope is controlled by moving the master robotic 

handles and it provides, unlike conventional laparoscopy, tridimensional view with adjustable magnification. 

At the console, the surgeon uses the robotic handles to move the tips of the instruments. All movements from the 

instrument controllers are transformed into electronic signals that are filtered of human hand tremor and scaled (up 

to five times) before being transmitted to the instrument tips. 

Dissection can be performed with the EndoWristTM mono polar cautery hook, different types of forceps with or 

without bipolar coagulation, shears. Larger vessels are controlled with needle holders or Harmonic Curved 

Shears. Most of the instruments can be reused utmost ten times. 

The main advantages of this system are the three dimensional view and the ability to scale motion and filter 

physiological hand tremor which allows precise dissection. The use of the robotic system in preset laboratory 

training models has been associated with faster performing times, increased accuracy, enhanced dexterity, faster 

suturing and reduced number of errors when compared with conventional laparoscopy. Complex procedures can be 

approached in a more efficient manner and the skills to perform them are acquired not only in a shorter time but also 

by a larger number of surgeons who have already encountered difficulties with conventional laparoscopy. 

Reduced morbidity, shorter recovery time and abbreviated hospital stay are to be listed among the benefits of 

laparoscopic surgery. Most of the procedures can now be performed in a minimally invasive manner. Nevertheless 

more complex surgeries are typically still managed by laparotomy. The main obstacle in accepting and widely 

applying minimally invasive techniques is the technical limitation of laparoscopic surgery. The drawbacks consist in 

impaired visualization due to the 2-D system and control of the visual field by the assistant moving the camera and 

light source. The response of the instrument tips to movement of the hands is reversed or counterintuitive. Suturing 

and knot tying are difficult because of limitations of access and of instrument motion. 

Since economic aspects are increasingly influencing medicine, cost analysis is an important and difficult task when 

evaluating any new technology. When establishing a robotic programme, there is a fixed cost associated with the 

purchase of a robotic surgical system and an annual maintenance fee for repairs and service. The other costs are: the 

cost of disposable robotic instruments and the cost of training new personnel and initial delays in setup time and 

procedure time during the learning curve and the training expenses up to the point the surgeon is certified. These 

costs are highly variable depending upon institutional and national health policies. However, the costs are still high 

and that is a limiting factor of the method dissemination. 

Robotic technology has emerged as a complement to laparoscopic surgery, one way to overcome its limitations. It 

offers a higher visibility, articulated tools that allow more sensitive surgical gestures and it broadens the perspective 

of executing minimally invasive interventions in better conditions (convenience for the surgical team, delicate 

dissection and easy suture). It also provides the opportunity to make minimally invasive interventions that otherwise 

would have been extremely difficult or even impossible to perform. 

ROBOTIC SPLENECTOMY 

The robotic splenectomy with the DaVinci surgical system is technically feasible and safe, with good results and 

without complications[1-4]. Robotic splenectomy probably will not replace the laparoscopic splenectomy for the 

most common indications like ITP or hemolytic anemia. It may be a very useful surgical tool in difficult 

splenectomy: partial splenectomy, splenectomy in liver cirrhosis, splenic tumors or malignant hemopathies. In these 

cases the robotic approach may shorten the operative time, decrease the blood loss and the risk of hemorrhagic 

complications during surgery. In addition, a minimally invasive splenectomy that is very difficult to be performed 

by classical laparoscopy[1,2], will be possible.

Robotic Splenectomy The Spleen 261 

Laparoscopic splenectomy is currently the procedure of choice for elective splenectomy and it is considered to be 

the "gold-standard" treatment of benign hematologic diseases, with normal or slightly enlarged spleens. However, 

the laparoscopic approach continues to raise certain technical challenges such as management of the massive spleen, 

splenectomy for portal hypertension and splenic malignancies and partial splenectomy. 

When a new procedure, especially one using new technology is performed, the surgical team has to answer a few 

questions: 

Could the surgical procedure (in this case the robotic splenectomy) be performed and is it feasible? 

If the answer is affirmative, then what are the advantages offered by the robotic splenectomy? 

The laparoscopic splenectomy is a successful surgical procedure. What are the indications for the 

robotic approach? 

After performing the first 30 total or subtotal splenectomies using the Da Vinci System, the authors indulge 

themselves to ascertain some advantages over conventional laparoscopy. The excellent viewing and superior 

maneuverability of the instruments are very important in difficult splenectomies: massive splenomegaly, liver 

cirrhosis, splenic tumors, and subtotal splenectomy. In these cases, primary ligation of the splenic artery, 

visualization of its branches and, generally, dissection in the splenic hilum can be performed with greater ease with a 

lower rate of hemorrhage incidents. 

The main haemostatic instruments (LigaSure Atlas, clip applier, Endo-GIA) are not available as robotic instruments 

and they have to be manipulated by the side-assistant surgeon through auxiliary trocars. On the other hand the 

ligations of the vascular pedicles are much easier with robotic instruments. 

The active augmentation of the abdominal cavity (laparo-lift: elevating the abdominal wall by the robotic camera 

arm which is actively held up by the camera trocar) makes the organ size less critical for the robotic approach. The 

superior maneuverability of the tips of the instruments inside the splenic hilum allows a more accurate dissection of 

the splenic vessels and identification of the pedicle of the remnant spleen increasing the rate of successful partial 

splenectomies. Furthermore, better visualization and maneuverability and motion control make the lysis of 

perisplenic adhesions more bloodless and safer than in the laparoscopic approach. 

Patient positioning, trocar and robot placement. The patient is positioned on the surgical table in a right lateral semidecubitus 

position on a 30 degree angle with the surgical table. The patient is then placed with the left hand as for 

the postero-lateral thoracotomy (Fig. 1). 

Figure 1: Patient position.

264 The Spleen, 2011, 264-275 

Splenic Trauma 

Takeshi Shimazu* 



CHAPTER 15 

Department of Traumatology and Acute Critical Medicine, Osaka University Faculty of Medicine (D-8), 2-15 

Yamadaoka, Suita-shi, Osaka, 565-0871, Japan 

Abstract: The spleen is one of the most frequently injured solid organs in blunt abdominal trauma [1]. In the 

history of trauma care, however, injuries of the spleen have received but scant attention compared to those of the 

liver and the kidney. Splenectomy has long been the preferred and standard treatment for bleeding from the spleen 

caused by blunt trauma, because the spleen was regarded as to have no vital function [2]. Owing to the pioneering 

article of King and Schumacher on the correlation between asplenia and overwhelming infection, the role of the 

spleen as an immunologic organ particularly in children, came to be widely recognized in the 1960s [3-6]. Then, 

splenic preservation treatment such as splenorrhaphy, partial splenectomy, and splenic embolisation, became the 

optimal management techniques for blunt splenic injury [7,8]. Due to the advances in CT imaging and 

angiography, nonoperative management (NOM) became the optimal management techniques for blunt splenic 

injury, and splenic embolisation is a valuable adjunct to the NOM [9,10]. 

EPIDEMIOLOGY 

Splenic injury is usually caused from blunt trauma, which could be as high as 95% in one series [11]. Blunt 

abdominal trauma affects more often solid organs rather than the bowel. The spleen is one of the most frequently 

injured organs in both adults and children (Fig. 1). Such injury can occur in motor vehicle accidents, falls, sports, 

and work-related accidents as a result of compressive forces and/or shearing forces produced by deceleration. 

Penetrating injury of the spleen can occur from stab wounds, gunshot wounds, shrapnel, spikes, broken bones, and 

other pointed objects. 

Injured spleen 

Figure 1: Splenic injury: A 25-year-old man presented after a motor vehicle accident. He collided with a car while driving a 

motorcycle, and was struck on the left side of the thorax and abdomen. He was in shock when he was transferred to the hospital. 

The FAST (focused abdominal sonogram for trauma) exam revealed left haemothorax and haemoperitoneum while vigorous fluid 

resuscitation was performed. Chest X-ray showed left haemopneumothorax and fractures of left 8-11 th ribs. As the 

haemodynamics remained unstable, he was taken to surgery. Eemergency laparotomy revealed severe splenic injury of AAST 

grade IV (Fig. 2) and vascular injuries of the mesocolon. Splenectomy was performed for the splenic injury. Post-operative 

course was uneventful. 

*Address correspondence to Takeshi Shimazu: Department of Traumatology and Acute Critical Medicine, Osaka University Faculty of 

Medicine (D-8), 2-15 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan; Tel: +81-6-6879-5707; Fax: +81-6-6879-5720; E-mail: shimazu@hpemerg.med.osaka-u.ac.jp

Splenic Trauma The Spleen 265 

The spleen is located in the left upper quadrant of the abdomen and is protected by the rib cage. Thus fracture of the 

left 9 th to 11 th ribs frequently accompanies splenic injury, while, in children splenic, rupture can occur without a rib 

fracture due to greater bone flexibility. Splenic injury occurs in 6 % to 30 % of reported blunt abdominal trauma 

patients, and is commonly associated with injuries of other visceral organs such as the liver and the bowel or other 

parts of the body [12,13]. Morbid and enlarged spleen from various disease state such as malaria and hematologic 

abnormalities are more susceptible to splenic injury even with minor trauma. 

CLASSIFICATION AND GRADING SYSTEMS 

Various classifications have been presented so far [13-19]. Early classifications included several factors such as the 

amount of intraabdominal bleeding. However, most classifications were based primarily on morphological patterns 

of the injured spleen obtained intraoperatively or by diagnostic imaging such as the computed tomography (CT), 

ultrasound or angiography. 

Aast Scaling System 

The most widely used grading system for blunt splenic injury is the Organ Injury Scale (OIS) described by the 

American Association for the Surgery of Trauma (AAST) [17]. Spleen OIS uses a scale of between grade I and 

grade V to indicate the increasing severity of splenic injury (Table 1), while grade VI injuries are, by definition, not 

salvageable. 

Grade I injuries are those with capsular tear or a minor parenchymal laceration. 

Grade II injuries involve capsular avulsion with minor parenchymal injury. 

Grade III involves a major parenchymal fracture or a major parenchymal laceration or completely 

penetration gunshot or stab wounds. 

Grade IV involves severe parenchymal stellate fractures, crush, bisection, or hilar injury. 

Grade V involves a completely shattered spleen. 

Table 1: The splenic organ injury scaling system of the AAST (1994 revision) (17) 

AST splenic injury scale (1994 Revision) 

Grade* Description AIS-90 

I Hematoma Subcapsular, < 10 % surface area 2 

Laceration Capsular tear, < 1cm parenchymal depth 2 

II Hematoma Subcapsular, 10-50% surface area 2 

Intraparenchymal, < 5 cm in diameter 2 

Laceration Capsular tear, 1-3 cm parenchymal depth which does not involve trabecular vessel 2 

III Hematoma Subcapsular, >50 % surface area or expanding 3 

Ruptured subcapsular or parenchymal hematoma 3 

Intraparenchymal hematoma >5 cm or expanding 3 

Laceration >3 cm parenchymal depth or involving trabecular vessels 3 

IV Laceration Involving segmental or hilar vessels producing 

major devascularization (>25% of spleen) 4 

V Laceration Completed shattered spleen 5 

Vascular Hilar injury which devascularizes the spleen 5 

*Advance one grade for multiple injuries up to grade III 

The AAST grading system is based on the estimated size of lacerations and hematomas as observed during 

laparotomy. Similar CT-based grading systems that have derived from the AAST scaling were also based on the 

anatomical patterns of the splenic injury. However, the CT findings and operative appearances are not always 

consistent with each other. The differences could be attributable in some cases to the evolution of the injury by the

266 The Spleen Takeshi Shimazu 

time of surgery after the CT scanning, but the major limitations of the AAST scaling system and similar CT-based 

systems were that they have not been reliable in predicting the outcome and guiding the management of blunt 

splenic injury [20]. 

CT Based Grading System 

Various CT based grading systems have been devised since the mid 1980s as the whole body CT scanners became 

clinically available. It is true that CT findings sometimes underestimate the degree of splenic injury, possibly related 

to a progression of bleeding found at surgery, and that CT findings may also overestimate the injury, but CT is an 

accurate method of identifying and quantifying splenic injury [16]. 

Recently, Marmery and the colleagues proposed a new grading system incorporating splenic vascular injury (Table 

2). With the use of contrast-enhanced multi-detector CT (MDCT), the new grading system adopted CT evidence of 

active splenic hemorrhage and vascular injuries which is predictive of the need for splenic arteriography and 

transcatheter embolisation or splenic surgery [21]. Patients with low-grade splenic injuries by the AAST 

classification would be upgraded to grade 4a or 4b in the new CT-based system if any signs of active bleeding or 

nonbleeding vascular injuries are observed. This grading system would contribute to predict the outcome and direct 

initial clinical management of patients with blunt splenic trauma [22]. 

Table 2: MDCT-based grading system for blunt splenic injury (Marmery 2007) (21) 

MDCT based grading by Marmery et al. (AJR 2007) 

Grade Criteria 

1 Subcapsular haematoma < 1 cm thick 

Laceration < 1cm parenchymal depth 

Parenchymal haematoma < 1 cm diameter 

2 Subcapsular haematoma 1 to 3 cm thick 

Laceration 1 to 3 cm in parenchymal depth 

Parenchymal haematoma 1 to 3 cm in diameter 

3 Splenic capsula disruption 

Subcapsular haematoma > 3 cm thick 

Laceration > 3 cm in parenchymal depth 

Parenchymal haematoma >3cm in diameter 

4a Active intraparenchymaland subcapsular splenic bleeding 

Splenic vascular injury (pseucoaneurysm or arteriovenous fistula) 

Shattered spleen 

4b Active intraparenchymal bleeding 

PATHOPHYSIOLOGY OF SPLENIC INJURY 

The two most important pathophysiologic concerns in patients with splenic injury are massive bleeding from the 

spleen in the acute phase, and subsequent immunosuppression that might lead to overwhelming infection in the 

postoperative periods for life. 

The spleen receives its arterial blood supply from the splenic artery, one of the major branches of the celiac axis, and 

also from the short gastric arteries and the left gastro-omental artery. Such abundant blood supply and its friable 

structure contribute to potential major blood loss in injury [23]. 

Minor lacerations and capsular tears that were not detected by initial evaluation and did not necessitate immediate 

interventions may slowly develop and lead to rupture and hemorrhage later. Delayed rupture of the spleen occurs in

276 The Spleen, 2011, 276-279 

A 

Index 

Abscess - 13-15, 42-44, 47, 81, 82, 85, 137, 147, 149, 156-159, 163, 165, 167, 170, 195, 206-208, 210, 219, 220, 

229, 230, 234, 238, 240, 244, 245, 256, 269, 270 

AIDS - 42, 79, 219, 230, 236, 251, 256, 260 

Amyloidosis - 46, 65, 66, 78, 137 

Anaemia - 4, 12, 13, 35, 47, 52-54, 58, 59, 61, 76, 78, 79, 81, 82, 88, 121, 139, 138, 141, 142, 149, 158, 159, 160, 

164, 167, 169, 179, 180-182, 194, 201-204, 207, 213, 219, 223-225, 231-233, 236, 240, 250251 

Angiogenesis - 108 

Angiosarcoma - 47, 59, 61, 62, 160, 192 

Autotransplantation - 87, 98, 101, 105, 108, 109, 188, 221, 241, 144, 269, 272 

Artery aneurism - 125, 142, 144, 145, 147, 143, 163-165, 167, 251. 

Asplenia - 31, 75, 87, 103, 219, 223, 224, 240, 267, 269 

B 

Billroth's cords - 6, 46, 75, 79, 80, 81, 123 

Biopsy - 37, 53, 169, 184, 197, 229 

Blood vessel - 24, 26, 58, 59, 65, 75, 99, 100, 117, 123, 154, 159, 203 

Burkitt - 193 

C 

Collateral circulation - 120, 121, 128, 134, 135, 137, 147 

Cyst - 12, 13, 15, 58, 59, 65, 76, 87, 147, 153, 157, 160, 164-167, 229, 232 

Cystadenoma - 154, 232 

Cytology - 50, 60, 162 

Cytopenia - 44, 47, 49, 54, 73, 138, 211, 219, 232, 236, 240 

D 

Dislipidaemia - 236 

Drepanocytosis - 13, 219, 233 

E 

Elyptocytosis - 219, 233 

Extracellular matrix - 24, 30 

F 

Faucher's disease - 9, 12-15, 88, 137 

Felty's syndrome - 81, 137, 251 

Fistula - 124, 136, 144, 145, 149, 153, 154, 164, 166, 167 

G 

Galen's duct - 6 

Growth factor - 100, 185, 213 

H 

Haematopoiesis - 8, 64, 137, 138, 162, 218 

Haemocateresis - 8 


All rights reserved - © 2011 Bentham Science Publishers Ltd.

Index The Spleen 277 

Haemorrhage - 7, 46, 61, 65, 76, 124, 138, 142, 144, 145, 155, 156, 159-161, 164, 167, 168, 169, 205, 222, 238, 

240, 243, 245, 257, 269 

Haemangioma - 14, 47, 57, 58, 59, 62, 82, 153-155, 159-161, 168, 170, 197, 219, 228, 234, 236 

Haematopoiesis - 8, 64, 134, 135, 137, 138, 162, 218 

Haemostasis - 129, 205, 208, 217, 238, 239, 243, 255, 263, 267 

Histology - 5, 21, 66, 88, 155, 161 

Histoplasmosis - 40, 79, 80 

Hodgkin's - 13, 40, 47, 54, 56, 57, 59, 61, 193, 211219, 225, 226, 235, 250-252 

Hydatic disease 41, 49 

Hyposplenism - 87, 103, 104, 

Hypersplenism - 7, 26, 43, 46, 65, 76, 77, 80, 82, 88, 121, 135, 138-144, 149, 160-162, 167, 179, 207, 219, 220, 222, 

225, 227, 232, 238, 240, 250, 256 

I 

Infact - 38, 43-45, 56, 58, 65, 77, 78, 82, 142, 145, 147, 149, 153, 154, 155, 158, 162, 163, 165, 169, 170, 195, 197, 

224, 230, 231, 238, 244, 252 

Ischaemia - 145, 146, 158, 231, 236, 244 

K 

Kaposi - 81. 

L 

Laparoscopic splenectomy - 149, 156, 197, 204, 205, 207, 209, 257, 260-262 

Leiomyosarcoma - 229 

Leishmaniosis - 80, 219, 220, 230 

Leukemia - 38, 44, 47, 48, 49, 51, -53, 55, 57, 65, 82, 88, 136, 137, 179, -181, 184, 187, 251, 252 

Leukocytosis - 158, 207, 213, 233, 238, 240 

Leukopenia - 148, 149, 222, 237 

Leukosarcoma -11 

Ligament - 6, 75, 118, 124, 127, 128, 137, 165, 169, 219, 220, 236, 241, 242, 252-254, 262 

Lymphangioma - 59, 82, 153-155, 159, 161, 162, 170, 197, 207 

Lymphatic vessel - 6, 91, 123, 161 

Lymphoma - 37, 47-51, 54-57, 59, 193, 207, 212, 220, 225, 226, 235, 236, 250, 252 

M 

Malpighi's capsule - 5 

Marginal zone - 22, 23, 25-32, 47-50, 56, 57, 89, 123, 193 

Myelofibrosis - 13, 45, 52, 65, 89, 142, 204, 224, 251 

Myeloid metaplasia - 13, 14, 64, 89, 187, 219, 225, 226, 240, 251 

Myeloid splenomegaly - 224, 225 

N 

Nerve - 6, 26, 33, 89, 122, 138, 205 

O 

Overwhelming post-splenectomy sepsis - 31, 103 

Overwhelming sepsis - 31, 142, 158, 240, 271 

P 

Pancytopenia - 53, 55, 61, 222, 224, 225


Partial splenectomy - 10, 12, 13, 15, 37, 84, 86, 88, 102, 128, 130, 142, 156, 157, 162, 187, 208, 221, 224-229, 232, 

243, 244, 260, 261, 269, 271, 272, 274 

Pathophysiology - 3 

Perifollicular zone - 23, 27 

Polycythemia - 45, 231, 251 

Portal hypertension - 12-14, 46, 76, 85, 88, 121, 122, 124-127, 162, 163, 166-170, 219, 220, 222, 223, 225, 233, 

234, 237, 238, 240-243, 250, 251, 261 

Post-operative - 37, 105, 135, 142, 145, 146, 157, 165, 187, 202-207, 211, 212, 218, 226, 237-239, 252, 255, 256, 

257, 264, 266 

Pre-operative - 47, 142, 145, 148, 160, 167, 201-205, 213, 237, 250, 252, 255 

Properdin - 20, 97, 104, 135, 218, 244, 271 

Purpura - 10, 12, 13, 79, 87, 88, 104, 139, 202, 204205, 218, 233, 250, 251 

R 

Repair - 125, 164, 165, 260 

Retarded growth - 231 

Robotic splenectomy - 259, 260-263 

S 

Sarcoidosis - 40, 80, 136, 137, 146, 251 

Sarcoma - 81, 147, 167, 193, 219, 236 

Schistosomiasis - 4, 5, 41, 77, 80, 137, 138, 219, 222, 225, 230 

Sickle - 43, 45, 78, 82, 158, 211, 223, 224, 231, 240 

Sinusoid - 6, 23, 40, 46, 78, 81, 85, 89, 92, 92, 93, 169 

Spherocytosis - 12, 13, 77, 82, 87, 88, 137, 205, 211, 223, 231, 233, 251, 271 

Splenic anatomy - 130, 257 

Splenic autoimplant - 101, 102, 108, 229, 231 

Splenic cord - 6, 20, 23, 51, 80, 85, 89, 123, 138 

Splenic implant - 14, 87, 98, 99, 100, 101-103, 105, 108, 188, 210, 212, 245 

Splenic morphology - 5 

Splenic pain - 148, 231, 236, 239 

Splenic pole - 13, 85, 118, 121, 129, 187, 217, 221, 223-228, 239, 242, 244, 262 

Splenic suture - 15 

Splenic vessels - 6, 14, 117, 122, 124, 156, 162, 171, 212, 231, 234, 242, 261 

Splenitis - 38, 40, 79, 81, 155 

Splenocytes - 33, 109, 233, 235 

Splenogastric artery - 121 

Splenogastric vein - 119, 126 

Splenogastric vessel - 6, 7, 13, 14, 15, 85, 88, 118, 121, 128, 129, 187, 217, 221, 223-225, 227, 239, 241, 242, 244 

Splenorrhaphy - 15, 34, 85, 208, 269, 271-273 

Splenosis - 14, 87, 88, 98, 100, 105, 209, 272 

Stem cell - 33, 64, 65, 81, 89, 93, 96, 108, 109, 182, 186, 187, 189, 203, 218 

Subtotal splenectomy - 13-15, 88, 109, 126, 129, 142, 187, 188, 221, 223-228, 231, 232, 239, 242-244, 261, 263 

Suture - 14, 15, 85, 124, 128, 129, 165, 207, 221, 222, 242, 243, 244, 245, 246, 255, 260 

Storage - 4, 8, 25, 80, 89, 194, 218, 222, 223, 225, 230, 232, 233 

T 

Thalassaemia - 13, 21, 82, 87, 88, 137, 205, 208, 213, 219, 223, 231, 240, 251, 252, 271 

Thrombocytopenia - 33, 47, 52, 53, 58, 59, 61, 76, 138-145, 148, 149, 179-182, 184, 194, 204, 205, 213, 225, 237, 

250 

Thrombocytosis - 32, 108, 141, 156, 158, 167, 204, 207, 210-213, 231, 233, 238, 256 

Toxoplasmosis - 40, 79, 80

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